th Annual Meeting of the PANCREAS CLUB · Welcome to the 48th Annual Meeting of the Pancreas Club...

48th Annual Meeting of the

PANCREAS CLUB

MAY 2-3, 2014WESTIN LOMBARD • CHICAGO, IL

WELCOME! Welcome to the 48th Annual Meeting of the Pancreas Club at the Westin Lombard in Chicago. The Mission of the Pancreas Club, since its founding in 1966, is to promote the interchange of ideas between pancreatologists throughout the world and to maintain an informal “club” atmosphere.

For the first time, the Pancreas Club is pleased to introduce an expanded two full-day program with the annual dinner taking place on Friday evening. Once again, we received over 200 abstracts which were reviewed by the Program Committee. We know that you will be fully engaged in both listening to the excellent presentations and in the discussions which follow. Posters of Distinctions will be presented by authors and addressed by leading faculty during the Poster Rounds with Professors. Authors will also be available posterside during the several Poster Sessions.

This meeting will offer continuing medical education credits through a joint sponsorship with the American College of Surgeons. We thank them for their support of this important meeting. We hope this provides a benefit to your CME needs and appreciate you support of this meeting

The abstracts selected for oral and poster presentation are included in this program book and are also available on our website.

DEAR MEMBERS AND GUESTS,Allow me to add my welcome to the 48th Annual Meeting of the Pancreas Club at The Westin Lombard Yorktown Center. The scientific program promises to be robust and stimulating. For those not attending the scientific sessions, there is much to do in the city of Lombard. Also known as Lilac Village, Lombard is famous for Lilacia Park which is an 8.5 acre horticultural showcase featuring 800 lilcas and 25,000 tulips. Lilac time runs from May 3 through May 18. For those that love to shop, the Westin Lombard is just steps from Yorktown Shopping Center where you can shop in such stores as Von Maur, JC Penney and Carson Pirie Scott. Further east is the second largest shopping center in the Chicago area, Oak Brook Center, located at the junction of 22nd Street and Route 83 in Oak Brook, Illinois and is home to Nordstrom, Lord & Taylor, Macy’s and Neiman Marcus, along with another 150+ stores. In addition to shopping, Lombard and Oak Brook offer many restaurants rated as Illinois best restaurants providing a wide variety of foods, such as, American, Asian, Bistro, Chinese, French, Italian, Mexican, sea food and vegetarian – so there is much to do in the short time you will be in town.

If moving on to downtown Chicago after the meeting, may I encourage you to take advantage of purchasing through registration a shuttle reservation for Saturday evening. We look forward to seeing all of you at the 48th Annual Meeting of the Pancreas Club for two days of science and fellowship.

Sincerely, Gerard V. Aranha, MD, FRCSC, (C), FACS

William H. Nealon, MD

Michael Farnell, MD

Gerard Aranha, MD

L. William Traverso, MD

PANCRE A SCLUB DIREC TORS

LOCAL ARRANGEMENTS CHAIR

TABLE OF CONTENTS

General Information 2

Accreditation & Disclosure Information 3

Schedule-at-a-Glance 6

2014 Annual Dinner Honoree: L. William Traverso, MD 8

Supporters & Exhibitors 9

Hotel Floorplan & Area Map 10

Scientific Program 11

Poster Listings 20

Oral Abstracts 37

2014 Membership Roster 108

Past & Future Meetings 151

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GENERAL INFORMATION

MEETING LOCATIONThe Westin Lombard Yorktown Center70 Yorktown Shopping Center Lombard, IL 60148

PHONE: 630-719-8000

MEETING HOURS

REGISTRATION Grand Ballroom Foyer

Thursday, May 1, 2014 • 6:00 pm – 8:00 pmFriday, May 2, 2014 • 6:30 am – 5:30 pmSaturday, May 3, 2014 • 6:45 am – 5:00 pm

SCIENTIFIC SESSIONS Grand Ballroom A-E with Posters in Grand Ballroom F-J

Friday, May 2, 2014 • 7:45 am – 5:30 pmSaturday, May 3, 2014 • 8:00 am – 4:45 pm

EXHIBITS Grand Ballroom F-J

Friday, May 2, 2014

9:30 am – 3:30 pm Exhibits Open9:30 am – 9:50 am Refreshment Break in Exhibit Area3:10 pm – 3:25 pm Refreshment Break in Exhibit Area

Saturday, May 3, 2014

9:30 am – 6:00 pm Exhibits Open9:45 am – 10:00 am Refreshment Break in Exhibit Area3:15 pm – 3:30 pm Refreshment Break in Exhibit Area4:45 pm – 6:00 pm Wine & Cheese Awards Reception

GENERAL BUSINESS MEETING Grand Ballroom A-E

Friday, May 2, 2014 • 5:30 pm – 6:00 pm

ANNUAL DINNER/RECEPTION Junior Ballroom

Friday, May 2, 2014 • 6:00 pm – 10:00 pm

AWARDS RECEPTION Grand Ballroom F-J

Saturday, May 3, 2014 • 4:45 pm – 6:00 pm

General Information 2 TABLE OF CONTENTS

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ACCREDITATION & DISCLOSURE INFORMATION

CONTINUING MEDICAL EDUCATION

MEETING/LEARNING OBJECTIVES At the conclusion of this meeting, participants will be able to:• Address the challenges of the management of all of the complexities of pancreatic

diseases with considerably greater insight and evidence-based decision making.• Understand the role of total pancreatectomy and islet autotransplant in

management of chronic pancreatitis.• Understand the methods for best practice in drain management following

pancreatectomy based upon prospective data.• Articulate the role of fine needle aspirate of neuroendocrine neoplasms of the

pancreas.• Understand the algorithm for management of postpancreatectomy

hemorrhage.• Understand the unique tumor biology of pancreatic carcinoma metastatic to

the lungs.• List additional/different treatment options for patients based on evidence

provided in abstract presentations.

ACCREDITATION STATEMENTThis activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the American College of Surgeons and the Pancreas Club. The American College of Surgeons is accredited by the ACCME to provide continuing medical education for physicians.

AMA PRA CATEGORY 1 CREDITS™The American College of Surgeons designates this live activity for a maximum of 15.25 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

PROGRAM COMMITTEE MEMBERSWilliam Nealon, MD, ChairGerard Aranha, MDMichael Farnell, MDJason Fleming, MDNipun Merchant, MDJames Moser, MD

William Traverso, MDMark Truty, MDChristopher Wolfgang, MDVictor Zaydfudim, MDNicholas Zyromski, MD

American College of Surgeons Division of Education



DISCLOSURE INFORMATION

In accordance with the ACCME Accreditation Criteria, the American College of Surgeons, as the accredited provider of this activity, must ensure that anyone in a position to control the content of the educational activity has disclosed all relevant financial relationships with any commercial interest. Therefore, it is mandatory that both the program planning committee and speakers complete disclosure forms. Members of the program committee were required to disclose all financial relationships and speakers were required to disclose any financial relationship as it pertains to the content of the presentations. The ACCME defines a ‘commercial interest’ as “any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients”. It does not consider providers of clinical service directly to patients to be commercial interests. The ACCME considers “relevant” financial relationships as financial transactions (in any amount) that may create a conflict of interest and occur within the 12 months preceding the time that the individual is being asked to assume a role controlling content of the educational activity.

ACS is also required, through our joint sponsorship partners, to manage any reported conflict and eliminate the potential for bias during the activity. All program committee members and speakers were contacted and the conflicts listed below have been managed to our satisfaction. However, if you perceive a bias during a session, please report the circumstances on the session evaluation form.

Please note we have advised the speakers that it is their responsibility to disclose at the start of their presentation if they will be describing the use of a device, product, or drug that is not FDA approved or the off-label use of an approved device, product, or drug or unapproved usage.

The requirement for disclosure is not intended to imply any impropriety of such relationships, but simply to identify such relationships through full disclosure and to allow the audience to form its own judgments regarding the presentation.

Accreditation & Disclosure Information 4 TABLE OF CONTENTS

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DISCLOSURES

SPEAKERS/MODERATORS/ CHAIRS/DISCUSSANTS

NOTHING TO DISCLOSE

DISCLOSURE As it pertains to the content of the presentation

Ashok Saluja Minneamrita - Stock options/ Partial ownership; Consulting

Carlos Fernandez del Castillo XCharles Vollmer XCharles Yeo XClaudio Bassi XDavid Adams XDouglas Evans XElisa Giovannetti XHiroki Yamaue XHoracio Asbun XKyoichi Takaori XMark Talamonti XMarshall Baker XMatthew Katz XMichael Kendrick XRoberto Coppola XSyed Ahmad XShuji Isaji XUgo Boggi XPLANNING COMMITTEE

NOTHING TO DISCLOSE

DISCLOSURE All commercial relationships

Christopher Wolfgang XGerard Aranha * XMichael Farnell * XJason Fleming * XNicholas Zyromski * XNipun B. Merchant XJames Moser * Abbvie - Honorarium;

Speaker/ panelMark Truty XVictor Zaydfudim * XWilliam Nealon * XWilliam Traverso X

*Indicates also moderator/faculty


MEETING ROOMSSCIENTIFIC SESSIONS: Grand Ballroom A-EPOSTERS: Grand Ballroom F-JREGISTRATION: Grand Ballroom FoyerEXHIBITS: Grand Ballroom F-J

THURSDAY, MAY 1, 20146:00 pm – 8:00 pm Exhibits/Poster Setup Grand Ballroom F-J

6:00 pm – 8:00 pm Registration Grand Ballroom Foyer

6:30 pm – 8:00 pm Advisory Committee Meeting/Dinner Cypress B

FRIDAY, MAY 2, 20146:30 am – 5:30 pm Registration Grand Ballroom Foyer

7:00 am – 7:45 am Continental Breakfast Grand Ballroom F-J

7:45 am – 8:00 am Welcome and Introductory Remarks Grand Ballroom A-E

8:00 am – 9:35 am SCIENTIFIC SESSION I Grand Ballroom A-E8:00 am TOPIC: Borderline Resectable Pancreatic Cancer8:35 am TOPIC: Neo-adjuvant Chemo Therapy/Radiation Therapy

9:30 am – 3:30 pm Exhibits Open Grand Ballroom F-J

9:30 am – 9:50 am Break with Exhibitors & Poster Viewing Grand Ballroom F-J

9:50 am – 11:00 am SCIENTIFIC SESSION II Grand Ballroom A-E TOPIC: Minimally Invasive Techniques/Screening for Cancer

11:00 am – 12:00 pm Poster Rounds with Professors Grand Ballroom F-J

12:00 pm – 1:00 pm Lunch Lilac Room

1:00 pm – 2:00 pm How I Do It Session Grand Ballroom A-E Borderline Resectable Adenocarcinoma of the Pancreas: Definitions and Management

2:00 pm – 3:10 pm SCIENTIFIC SESSION III Grand Ballroom A-E TOPIC: Translational Studies

3:10 pm – 3:25 pm Break with Exhibitors & View Posters Grand Ballroom F-J

3:25 pm – 5:30 pm SCIENTIFIC SESSION IV Grand Ballroom A-E3:25 pm TOPIC: Pancreatitis4:45 pm TOPIC: Neuroendocrine Tumors

5:30 pm – 6:00 pm Pancreas Club Brief Business Meeting Grand Ballroom A-E

6:00 pm – 10:00 pm Pancreas Club Annual Dinner/Reception Junior Ballroom

Schedule-at-a-Glance

SCHEDULE-AT-A-GLANCE

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SATURDAY, MAY 3, 20146:45 am – 5:00 pm Registration Grand Ballroom Foyer


8:00 am – 9:45 am SCIENTIFIC SESSION V Grand Ballroom A-E TOPIC: IPMN



10:00 am – 11:00 am SCIENTIFIC SESSION VI Grand Ballroom A-E TOPIC: Cancer Basic

11:00 am – 12:00 pm Poster Rounds with Professors Grand Ballroom F-J


1:00 pm – 3:15 pm SCIENTIFIC SESSION VII Grand Ballroom A-E1:00 pm TOPIC: Early Complications After Pancreatico-Duodenectomy/Drains & Fistulas2:15 pm TOPIC: Quality/Predictors/Regionalization


3:30 pm – 4:45 pm SCIENTIFIC SESSION VIII Grand Ballroom A-E3:30 pm TOPIC: Quality/Predictors/Regionalization (continues)4:10 pm TOPIC: Late Postoperative Issues

4:45 pm – 6:00 pm Wine & Cheese Awards Reception Grand Ballroom F-J

SCHEDULE-AT-A-GLANCE

Schedule-at-a-Glance

AWARDSThe Pancreas Club will recognize three outstanding presentations. They will be awarded during the closing, Saturday afternoon, reception:

• PANCAN RESEARCH AWARD: $1,000 for the best oral presentation of pancreatic cancer research by a resident or fellow. This award is generously funded by the Pancreatic Cancer Action Network.

• KENNETH WARREN/PANCREAS CLUB RESEARCH AWARD: $1,000 for the best oral presentation of clinical or basic science pancreatitis by a resident or fellow. This award is generously funded by the Pancreas Club and the Kenneth Warren Foundation.

• JOHN HOWARD RESEARCH AWARD: $1,000 for the best presentation from young junior faculty, who is within 5 years of their end of residency. This award is generously funded by the Arpa Foundation.

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2014 ANNUAL DINNER HONOREE

L. WILLIAM TRAVERSO, MDPRESENTED BY: Richard Kozarek, MD, Virginia Mason Medical Center, Seattle, WA

Bill Traverso has been a member of the Pancreas Club since 1978 and a Director since 1999. His undergraduate degree was received at the University of Nevada, while his M.D. degree and residency training were both completed at the UCLA School of Medicine, Los Angeles. His interest in the pancreas was fostered by his mentors at UCLA: William Longmire and Ron Tompkins. The first pylorus-preserving pancreatoduodenectomy was performed on February 28,

1977 for a patient with chronic pancreatitis. To this day, the procedure is commonly known as the Traverso-Longmire operation.

Dr. Traverso’s primary interest has been surgical management of pancreatic disease. He has published over 260 peer-reviewed articles or book chapters and has made over 300 national and international podium presentations. Dr. Traverso has served as President of the Society of American Gastrointestinal and Endoscopic Surgeons, the Society for Surgery of the Alimentary Tract, the North Pacific Surgical Association and the American College of Surgeons Washington Chapter. Since 1997, he has been a director for the Japanese Society of Hepatobiliary and Pancreatic Surgery Observership.

Dr. Traverso has organized a number of international symposia on pancreatic cancer beginning first in 2001 in Seattle, followed by meetings in Pisa, Rome, Kyoto and an upcoming meeting in July 2014 in Verona, Italy. He has fostered relationships with pancreatophiles across the world as evidenced by the strong international representation at the annual Pancreas Club meeting. Bill helped build a center of excellence for hepatobiliary and pancreatic disease in his long career at Virginia Mason Medical Center from 1984-2010. He continues as a leader in pancreatic surgery in his current position at St. Luke’s Health System, Center for Pancreatic and Liver Disease, Boise, Idaho. The growth and vitality of the Pancreas Club has been in no small measure due to his efforts. Please join us as we honor Bill at the Pancreas Club annual dinner.

PAST ANNUAL DINNER HONOREES2012 Howard Reber, MD2011 Edward Bradley, III, MD2010 Hans Beger2009 Prof. Seiki Matsuno2008 Andy Warshaw, MD2007 Charles Frederick Frey, MD2005 John M. Howard, MD2004 John Cameron, MD and Fujio Hanyu, MD

2014 Annual Dinner Honoree 8 TABLE OF CONTENTS

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SUPPORTERS & EXHIBITORS

The Pancreas Club gratefully acknowledges support for the 48th Annual Pancreas Club Meeting from the following:

EDUCATIONAL GRANT SUPPORT

PLATINUM

SILVER

BRONZE

EXHIBITORSAbbVie

Celgene Corporation

Ethicon

Forest Pharmaceuticals, Inc.

Medtronic Advanced Energy

RedPath Integrated Pathology, Inc.

Vector Surgical, LLC

AWARDS SUPPORT• Pancreatic Cancer Action Network

In support of PanCan Research Award

• Kenneth Warren Foundation In support of Kenneth Warren/Pancreas Club Research Award

• The Pancreas Club In support of Kenneth Warren/Pancreas Club Research Award

• Arpa Foundation In support of John Howard Research Award

Supporters & Exhibitors 9

Hotel Floorplan & Area Map

HOTEL FLOORPLAN & AREA MAP

THE WESTIN LOMBARD YORKTOWN CENTER

290

290294

90

12

41

Westin LombardYorktown Center

26 MILES

19 M

ILES

Chicago O’HareInternational

Airport

Chicago

AREA MAP & LOCAL TRANSPORTATIONThe Westin Lombard is located 26 miles from downtown Chicago (DDW hotels). For your convenience, you have an option of purchasing shuttle reservation for Saturday evening, after the PC meeting to downtown Chicago. Please stop by the registration desk to purchase your ticket by 3:00 pm on Friday. Hurry, space is limited!

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SCIENTIFIC PROGRAM

FRIDAY, MAY 2, 20146:30 am – 5:30 pm Registration Grand Ballroom Foyer


7:45 am – 8:00 am Welcome and Introductory Remarks Grand Ballroom A-E

William H. Nealon, MD, Vanderbilt University, Nashville, TN William Traverso, MD, St. Luke’s Hospital, Boise, ID Michael Farnell, MD, Mayo Clinic, Rochester, MN

8:00 am – 9:35 am SCIENTIFIC SESSION I Grand Ballroom A-E MODERATORS: Douglas Evans, MD & Shuji Isaji, MD

TOPIC: Borderline Resectable Pancreatic Cancer

8:00 am S001 DIAGNOSTIC LAPAROSCOPY TO DETECT OCCULT METASTATIC DISEASE PRIOR TO NEOADJUVANT CHEMORADIATION IN BORDERLINE RESECTABLE PANCREATIC DUCTAL ADENOCARCINOMA – A COST ANALYSIS – June S. Peng (Long)

8:15 am S002 RISK OF VENOUS THROMBOEMBOLISM DURING NEOADJUVANT THERAPY FOR RESECTABLE AND BORDERLINE RESECTABLE (BLR) PANCREATIC ADENOCARCINOMA (PC) – A. N. Krepline (Long)

8:30 am S003 IMPACT OF SURGICAL RESECTION AFTER CHEMORADIOTHERAPY FOR LOCALLY ADVANCED UNRESECTABLE PANCREATIC DUCTAL ADENOCARCINOMA – Masashi Kishiwada, PhD, MD (Short)

TOPIC: Neo-adjuvant Chemo Therapy/Radiation Therapy

8:35 am S004 A COMPREHENSIVE ASSESSMENT OF NEOADJUVANT THERAPY FOR PANCREATIC ADENOCARCINOMA: RESULTS FROM THE NATIONAL CANCER DATABASE (NCDB) – Russell S. Lewis, BS (Long)

8:50 am S005 DOES THE USE OF NEOADJUVANT THERAPY FOR PANCREATIC ADENOCARCINOMA INCREASE POSTOPERATIVE MORBIDITY AND MORTALITY RATES? – Amanda B. Cooper, MD (Long)

9:05 am S006 NEOADJUVANT CHEMORADIATION VERSUS NEOADJUVANT CHEMOTHERAPY PRIOR TO PANCREATICODUODENECTOMY FOR PANCREATIC CANCER – Pragatheeshwar Thirunavukarasu, MD (Long)


SCIENTIFIC PROGRAM

Scientific Program

9:20 am S007 CHANGES IN BODY COMPOSITION DURING PREOPERATIVE THERAPY FOR RESECTABLE PANCREATIC CANCER: DO THEY MATTER? – Amanda B. Cooper, MD (Short)

9:25 am S008 PROSPECTIVE RANDOMIZED CONTROLLED STUDY COMPARING OUTCOME BETWEEN STANDARD RESECTION AND AN EXTENDED RESECTION THAT INCLUDED DISSECTION OF THE NERVE PLEXUS AND VARIOUS LYMPH NODES IN PATIENTS WITH PANCREATIC HEAD CANCER – Jin-Young Jang (Short)

9:30 am S009 MICROSCOPIC RESIDUAL TUMOR AFTER PANCREATICODUODENECTOMY FOR CANCER. PRELIMINARY RESULTS OF A MULTICENTRIC PROSPECTIVE RANDOMIZED TRIAL – Roberto Coppola, MD, FACS (Short)



9:50 am – 11:00 am SCIENTIFIC SESSION II Grand Ballroom A-E MODERATORS: Horacio Asbun, MD & Ugo Boggi, MD

TOPIC: Minimally Invasive Techniques/Screening for Cancer

9:50 am S010 MINIMALLY INVASIVE PANCREATODUODENECTOMY: IS THE LEARNING CURVE SURMOUNTABLE? – Attila Nakeeb, MD (Long)

10:05 am S011 TOTAL LAPAROSCOPIC PANCREATICODUODENECTOMY FOR PANCREATIC DUCTAL ADENOCARCINOMA: ONCOLOGIC ADVANTAGES OVER OPEN APPROACHES? – Kristopher P. Croome, MD, MS (Long)

10:20 am S012 PRELIMINARY RESULTS OF A SWEDISH, MR BASED, SCREENING PROGRAM FOR INDIVIDUALS AT RISK FOR PANCREAS CANCER – Marco Del Chiaro, MD, PhD (Long)

10:35 am S013 EARLY DETECTION OF PANCREATIC INTRAEPITHELIAL NEOPLASIA USING NON-INVASIVE IMAGING TO LOCALIZE AND GRADE PROTEASE ACTIVITY – Dana A. Dominguez, BS (Long)

11:00 am – 12:00 pm Poster Rounds with Professors Grand Ballroom F-J PROFESSORS: Michael Kendrick, MD & Nicholas Zyromski, MD

See page 20 for list of posters. First 10 Posters marked with ★ : Authors will be by their posters to discuss their research poster presentations and Professor will lead short Q&A.


TABLE OF CONTENTS


1:00 pm – 2:00 pm HOW I DO IT SESSION Grand Ballroom A-E

Borderline Resectable Adenocarcinoma of the Pancreas: Definitions and ManagementMODERATORS: Jason Fleming, MD & Mark Talamonti, MD

This session is directed at practitioners who take care of patients with pancreatic cancer. In it we will discuss the management options for patients with pancreatic cancer who may or may not be suitable for surgical resection.

At the conclusion of this session, the attendees will be able to:

• Interpret diagnostic imaging results in patients with pancreatic cancer.

• Choose management approaches for patients with pancreatic cancer.

• Employ evidence-based principles of management in patient with pancreatic cancer.

Outline:

• Initial surgical resection of a PC patient with superior mesenteric vein involvement – Charles Vollmer, MD (8 min.)

• Preoperative therapy of a PC patient with superior mesenteric vein involvement – Syed Ahmad, MD (8 min.)

• Initial surgical resection of a frail PC patient with a resectable primary tumor – Charles Yeo, MD (8 min.)

• Preoperative therapy of a frail PC patient with a resectable primary tumor – Matthew HG Katz, MD (8 min.)

• Discussion (28 min.)

2:00 pm – 3:10 pm SCIENTIFIC SESSION III Grand Ballroom A-E MODERATORS: Ashok Saluja, MD & Kyoichi Takaori, MD

TOPIC: Translational Studies

2:00 pm S014 ROLE OF CYB5A IN PANCREATIC CANCER: CORRELATION WITH CLINICAL OUTCOME AND FUNCTIONAL CHARACTERIZATION IN THE MODULATION OF AUTOPHAGY AND ONCOGENIC PHENOTYPES – Elisa Giovannetti, MD, PhD (Long)

2:15 pm S015 CA 19-9 RESPONSE TO NEOADJUVANT THERAPY PREDICTS OUTCOME IN PANCREATIC ADENOCARCINOMA – Brian A. Boone, MD (Long)

Scientific Program

SCIENTIFIC PROGRAM

13

2:30 pm S016 DETECTION OF CLINICALLY RELEVANT GENETIC ALTERATIONS IN FINE NEEDLE ASPIRATES OF PANCREATIC CANCER IS POSSIBLE USING NEXT-GENERATION SEQUENCING – Vicente Valero III, MD (Long)

2:45 pm S017 NEW PLATFORMS FOR PDAC PRECLINICAL STUDIES: 3D TISSUE-ENGINEERED MODELS BASED ON PRIMARY CANCER CELLS AND SYNTHETIC SCAFFOLDS – Claudio Ricci, PhD (Long)

3:00 pm S018 BIOLUMINESCENT ORTHOTOPIC PANCREATIC-DUCTAL-ADENOCARCINOMA (PDAC) MOUSE MODELS DERIVED FROM PRIMARY PDAC CELLS AS A PLATFORM FOR THERAPEUTIC DISCOVERY – Niccola Funel, PhD (Short)

3:05 pm S019 COUNTERACTING CANCER CELL SURVIVAL STRATEGY: SENSITIZATION OF PANCREATIC CANCER CELLS TO TRAIL INDUCED CELL DEATH BY JAK2/STAT3 PATHWAY INHIBITION BY PREVENTING DEATH RECEPTOR DOWNREGULATION – Kaustav Majumder, MD (Short)


3:25 pm – 5:30 pm SCIENTIFIC SESSION IV Grand Ballroom A-E MODERATORS: Gerard Aranha, MD & David Adams, MD

TOPIC: Pancreatitis

3:25 pm S020 TOTAL PANCREATECTOMY WITH ISLET AUTOTRANSPLANTATION FOR CHRONIC PANCREATITIS: THE PRICE PATIENTS PAY FOR IMPROVEMENTS IN QUALITY OF LIFE – Katherine Morgan, MD (Long)

3:40 pm S021 COST-EFFECTIVENESS OF TOTAL PANCREATECTOMY WITH ISLET CELL AUTOTRANSPLANTATION FOR THE TREATMENT OF SMALL DUCT CHRONIC PANCREATITIS – Daniel E. Abbott, MD (Long)

3:55 pm S022 HIGH READMISSION RATES FOLLOWING SURGERY FOR CHRONIC PANCREATITIS – A. V. Fisher (Long)

4:10 pm S023 PANCREATICODUODENECTOMY FOR CHRONIC PANCREATITIS: A LONG-TERM FOLLOW-UP – Kristopher P. Croome, MD (Short)

4:15 pm S024 RISK OF RECURRENT PANCREATITIS AND PROGRESSION TO CHRONIC PANCREATITIS AFTER ACUTE PANCREATITIS – Usama Ahmed Ali, MD, MSc (Long)

SCIENTIFIC PROGRAM

Scientific Program 14 TABLE OF CONTENTS

TABLE OF CONTENTS

4:30 pm S025 SEVERE ACUTE PANCREATITIS: USING A MULTIDISCIPLINARY PERCUTANEOUS DRAINAGE PROTOCOL THE MAIN PREDICTOR OF HOSPITAL LENGTH OF STAY IS AMYLASE OR BACTERIA IN THE PERCUTANEOUS ASPIRATE – M. Sugimoto, MD (Long)

TOPIC: Neuroendocrine Tumors

4:45 pm S026 SURGICAL RESECTION PROVIDES A SIGNIFICANT OVERALL SURVIVAL BENEFIT FOR PATIENTS WITH SMALL PANCREATIC NEUROENDOCRINE TUMORS – Susan M Sharpe, MD (Long)

5:00 pm S027 RISK OF MALIGNANCY IN RESECTED NONFUNCTIONING PANCREATIC NEUROENDOCRINE TUMORS – Michael J. Ferrara, MS (Long)

5:15 pm S028 AN INVESTIGATION OF THE UTILITY OF KI-67 EXPRESSION IN PANCREATIC NEUROENDOCRINE TUMOUR FINE NEEDLE ASPIRATION SAMPLES – Nigel B. Jamieson, MD, PhD (Short)

5:20 pm S029 THE GASTRINOMA TRIANGLE REVISITED: DUODENAL WALL GASTRINOMA AND PANCREATIC GASTRINOMA LOCATIONS PREDICT BIOLOGICAL BEHAVIOR AND LONGEVITY – Sam G. Pappas, MD (Short)

5:25 pm S030 PATTERNS OF PRACTICE AND SURVIVALamONG PATIENTS WITH NON-METASTATIC PANCREATIC NEUROENDOCRINE TUMORS UNDER 2 CM – Jan Franko, MD, PhD (Short)

5:30 pm – 6:00 pm Pancreas Club Brief Business Meeting Grand Ballroom A-E

6:00 pm – 10:00 pm Pancreas Club Annual Dinner/Reception Junior Ballroom DINNER HONOREE: L. William Traverso, MD See page 8 for details.

SCIENTIFIC PROGRAM


SATURDAY, MAY 3, 20146:45 am – 5:00 pm Registration Grand Ballroom Foyer


8:00 am – 9:45 am SCIENTIFIC SESSION V Grand Ballroom A-E MODERATORS: Carlos Fernandez del Castillo, MD & Claudio Bassi, MD

TOPIC: IPMN

8:00 am S031 RE-CLASSIFICATION OF COMBINED-TYPE IPMNS ALLOWS FOR A BETTER DEFINITION OF TWO DISEASE ENTITIES – Giovanni Marchegiani, MD (Long)

8:15 am S032 CLINICAL VALIDATION OF NEW INTERNATIONAL CONSENSUS GUIDELINES FOR THE RESECTION OF BRANCH DUCT TYPE INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS (BD-IPMN) – Jin-Young Jang (Long)

8:30 am S033 INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM OF THE PANCREAS, ONE MANIFESTATION OF A MORE SYSTEMIC DISEASE? – Alexandra M. Roch, MD (Long)

8:45 am S034 THE BIOLOGY OF SMALL IPMN CANCERS (< 20 MM INVASIVE COMPONENT): A MULTI-INSTITUTIONAL ANALYSIS – Jordan M. Winter, MD (Long)

9:00 am S035 A NATIONAL PERSPECTIVE OF INVASIVE INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM (IPMN) – Russell S. Lewis, BS (Long)

9:15 am S036 CHARACTERIZATION OF PANCREATIC STROMAL CELLS ISOLATED FROM PANCREATITIS AND PANCREATIC ADENOCARCINOMA SURGICAL SPECIMENS – Daniel Delitto, MD (Short)

9:20 am S037 CURRENT INDICATIONS FOR SURGERY OF IPMN’S MAY OVERLOOK SOME PATIENTS WITH CANCER: RECOMMENDATIONS FOR CHANGE – Andrew H. Nguyen (Short)

9:25 am S038 MAIN PANCREATIC DUCT SIZE AND RISK OF MALIGNANCY IN INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM – Neda Rezaee, MD (Short)

9:30 am S039 DOES EUS IMPROVE OUTCOME IN SURVEILLANCE OF NON-RESECTED PRESUMED BRANCH-DUCT INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS? – Anna C. Evans, MD (Short)

SCIENTIFIC PROGRAM


TABLE OF CONTENTS

9:35 am S040 RESECTED PANCREATIC ADENOCARCINOMAS WITH RECURRENCE LIMITED IN LUNG HAVE A SIGNIFICANTLY BETTER PROGNOSIS THAN THOSE WITH OTHER RECURRENCE PATTERNS – Lei Zheng, MD, PhD (Short)

9:40 am S041 THE INDOLENT NATURE OF PULMONARY METASTASES FROM PANCREATIC CANCER – Stephanie Downs-Canner, MD (Short)



10:00 am – 11:00 am SCIENTIFIC SESSION VI Grand Ballroom A-E MODERATORS: James Moser, MD & Elisa Giovannetti, MD

TOPIC: Cancer Basic

10:00 am S042 PANCREATIC STELLATE CELL SECRETED IL-6 MEDIATES STAT3 DEPENDENT CANCER CELL INVASION – Jason A. Castellanos, MD (Long)

10:15 am S043 NEUTROPHIL EXTRACELLULAR TRAPS (NETS) ARE UPREGULATED IN PANCREATIC CANCER AS A RESULT OF AUTOPHAGY AND CONTRIBUTE TO HYPERCOAGULABILITY – Brian A. Boone, MD (Long)

10:30 am S044 ISOLATION AND CHARACTERIZATION OF DCLK1+ TUMOR CELLS OF PANCREATIC ADENOCARCINOMA PATIENTS – Jeremy L. Irvan, MD (Long)

10:45 am S045 SEQUENCE ALTERATIONS IN THE WEE1 NON-CODING REGION IS A FACILITATOR AND MARKER FOR PANCREATIC TUMORIGENESIS – Jordan M. Winter, MD (Short)

10:50 am S046 CHEMOTHERAPY RESISTANT PANCREATIC CANCER TUMOR-ASSOCIATED FIBROBLASTS ARE PROTUMORIGENIC – Paul A. Toste, MD (Short)

10:55 am S047 PTK6 INCREASES APOPTOSIS WITH GEMCITABINE TREATMENT IN PANCREATIC CANCER CELLS BY ENHANCING DNA DAMAGE – Hiroaki Ono, MD, PhD (Short)

11:00 am – 12:00 pm Poster Rounds with Professors Grand Ballroom F-J PROFESSORS: Marshall Baker, MD & Victor Zaydfudim, MD

See page page 29 for list of posters. First 10 Posters marked with ★ : Authors will be by their posters to discuss their research poster presentations and Professor will lead short Q&A.

SCIENTIFIC PROGRAM



1:00 pm – 3:15 pm SCIENTIFIC SESSION VII Grand Ballroom A-E MODERATORS: Michael Farnell, MD & Hiroki Yamaue, MD

TOPIC: Early Complications After Pancreatico-duodenectomy/Drains & Fistulas

1:00 pm S048 THE VALUE OF DRAINS AS A FISTULA MITIGATION STRATEGY FOR PANCREATODUODENECTOMY: SOMETHING FOR EVERYONE? RESULTS OF A RANDOMIZED PROSPECTIVE MULTI-INSTITUTIONAL STUDY – Matthew T. McMillan, BA (Long)

1:15 pm S049 A RANDOMIZED PROSPECTIVE MULTICENTER TRIAL OF PANCREATICODUODENECTOMY WITH AND WITHOUT ROUTINE INTRAPERITONEAL DRAINAGE – George Van Buren, II, MD (Long)

1:30 pm S050 RISK-ADJUSTED OUTCOMES OF CLINICALLY-RELEVANT POSTOPERATIVE FISTULA FOLLOWING PANCREATODUODENECTOMY: A MODEL FOR PERFORMANCE EVALUATION – Charles M Vollmer, MD (Long)

1:45 pm S051 HIGH PERFORMING WHIPPLE PATIENTS: FACTORS ASSOCIATED WITH SHORT LENGTH OF STAY AFTER OPEN PANCREATICODUODENECTOMY – Grace C Lee, BS (Long)

2:00 pm S052 THE ASSOCIATION BETWEEN PANCREATIC FISTULA GRADE C AND SURVIVAL AFTER PANCREATIC RESECTION FOR PANCREATIC CANCER – Manabu Kawai, MD, PhD (Short)

2:05 pm S053 DOES DRAIN FLUIDamYLASE ACCURATELY PREDICT PANCREATIC FISTULA? – Christina W. Lee, MD (Short)

2:10 pm S054 EARLY DRAIN REMOVAL: THE MIDDLE GROUND BETWEEN THE DRAIN VERSUS NO DRAIN DEBATE IN PATIENTS UNDERGOING PANCREATICODUODENECTOMY. A PROSPECTIVE VALIDATION STUDY – Zhi Ven Fong, MD (Short)

TOPIC: Quality/Predictors/Regionalization

2:15 pm S055 THE HYSLAR TRIAL: A PROSPECTIVE RANDOMIZED TRIAL ON THE USE OF A RESTRICTIVE FLUID REGIMEN WITH 3% HYPERTONIC SALINE (HS) VERSUS LACTATED RINGERS (LR) IN PATIENTS UNDERGOING PANCREATICODUODENECTOMY (PD) – Harish Lavu, MD (Long)

2:30 pm S056 CURRENT MANAGEMENT OF DELAYED BLEEDING AFTER PANCREATICODUODENECTOMY – Young Joon Ahn, PhD (Long)

SCIENTIFIC PROGRAM


TABLE OF CONTENTS

2:45 pm S057 BILE-CULTURE BASED ANTIMICROBIAL PROPHYLAXIS REDUCES SURGICAL SITE INFECTIONS (SSIS) IN PANCREATIC SURGERY – Alessandro Zerbi, MD (Long)

3:00 pm S058 IT IS QUALITY AND QUANTITY: A SINGLE INSTITUTION’S EXPERIENCE IN QUALITY MEASURES OF PANCREATIC CANCER CARE – Melanie Ongchin, MD (Long)


3:30 pm – 4:45 pm SCIENTIFIC SESSION VIII Grand Ballroom A-E MODERATORS: William Nealon, MD & Roberto Coppola, MD

TOPIC: Quality/Predictors/Regionalization (continues)

3:30 pm S059 MOBILE RISK CALCULATOR APP FOR OPERATIVE AND ONCOLOGIC OUTCOMES IN PATIENTS CONSIDERING PANCREADICODUODENECTOMY FOR PANCREATIC ADENOCARCINOMA – Steven Nurkin, MD (Short)

3:35 pm S060 PREDICTORS OF EARLY READMISSION AFTER PANCREATECTOMY – Caitlin W Hicks, MD, MS (Short)

3:40 pm S061 HIGH-VOLUME SURGEONS VERSUS HIGH-VOLUME HOSPITALS: ARE BEST OUTCOMES MORE DUE TO WHO OR WHERE? – Prashant B. Sukharamwala, MD (Long)

3:55 pm S062 WHAT ARE THE FINANCIAL IMPLICATIONS OF CENTERS FOR REGIONAL HEALTHCARE? – Alexander S. Rosemurgy, MD (Long)

TOPIC: Late Postoperative Issues

4:10 pm S063 THE INCIDENCE OF PANCREATOGENIC DIABETES AFTER MAJOR PARTIAL PANCREATIC RESECTION MAY BE GREATER THAN YOU THINK – Richard A. Burkhart, MD (Long)

4:20 pm S064 EFFECT OF HIGH-DOSE PANCREATIC ENZYME REPLACEMENT THERAPY ON THE DEVELOPMENT OF NON-ALCOHOLIC FATTY LIVER DISEASE AFTER PANCREATICODUODENECTOMY, PAYING ATTENTION TO ETIOLOGY OF DISEASES AND THE REMNANT PANCREATIC VOLUME – Rie Sato (Short)

4:45 pm – 6:00 pm Wine & Cheese Awards Reception Grand Ballroom F-J Presentation of three $1,000 awards (2 for resident/fellow; 1 for junior faculty) Closing Remarks

SCIENTIFIC PROGRAM


Poster Listings

POSTER LISTINGS

All posters located in Grand Ballroom F-J.

The ★ symbol indicates Poster of Distinction and they will be identified on the poster board by GOLD dot. Authors will be available for short oral presentations during the Poster Rounds with Professors.

Complete Poster Abstract descriptions are available online at www.pancreasclub.com.

FRIDAY, MAY 2, 2014★P001 THE CLINICAL VALUE OF PERITONEAL CYTOLOGY IN 984 PATIENTS WITH PANCREATIC CANCER WHO UNDERWENT CURATIVE RESECTION Sohei Satoi, MD, FACS, Fuyuhiko Motoi, MD, Kenichiro Uemura, MD, Manabu Kawai, MD, Masanao Kurata, MD, Masayuki Sho, MD, FACS, Ippei Matsumoto, MD, Hiroaki Yanagimoto, MD, Michiaki Unno, MD, Hiroki Yamaue, MD, Goro Honda, MD, FACS, Yoshiyuki Nakajima, MD, Makoto Shinzeki, MD, A-Hon Kwon, MD, Yoshiaki Murakami, MD, Multicenter Study Group of Pancreatobiliary Surgery in Japan, Osaka, JP

★P002 A 30-YEARS CELEBRATION OF FIRST DESCRIPTION OF CENTRAL PANCREATECTOMY (THE DAGRADI-SERIO-IACONO OPERATION): HISTORICAL OUTLINE AND SURGICAL OUTCOME Calogero Iacono, MD, Andrea Ruzzenente, MD, PhD, Simone Conci, MD, PhD, Claudio Bacchelli, MD, Tommaso Campagnaro, MD, Alessandro Valdegamberi, MD, Corrado Pedrazzani, MD, Francesca Bertuzzo, MD, Alfredo Guglielmi, MD, Department of Surgery - Division of General Surgery A - Unit of Hepato-Pancreatico-Biliary-Surgery - University of Verona Medical School, Verona, Italy., Verona, IT

★P003 MORBIDITY AND MORTALITY OF PANCREATICODUODENECTOMY FOR PREMALIGNANT PANCREATIC NEOPLASMS Timothy E Newhook, MD, Damien J LaPar, MD, MSc, James M Lindberg, MD, Todd W Bauer, MD, Reid B Adams, MD, Victor M Zaydfudim, MD, MPH, University of Virginia, Charlottesville, US

★P004 PANCREATICODUODENECTOMY IN FLORIDA: DO 20 YEAR TRENDS DOCUMENT SALUTARY BENEFITS OF CENTRALIZATION OF CARE? Thomas W Wood, MD, Sharona B Ross, MD, Amanda E Smart, Carrie E Ryan, MS, Prashant B Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

★P005 DEFINING TREATMENT AND OUTCOMES OF HEPATICOJEJUNOSTOMY FAILURE FOLLOWING PANCREATICODUODENECTOMY Richard A Burkhart, MD, Daniel Relles, MD, Danielle M Pineda, MD, Patricia K Sauter, Ernest L Rosato, MD, Harish Lavu, MD, Charles J Yeo, MD, Jordan M Winter, MD, Department of Surgery, Jefferson Pancreas, Biliary, and Related Cancer Center, Thomas Jefferson University, Philadelphia, PA, Philadelphia, US

★P006 A SERVICE BASED MID LEVEL PROVIDER UTILIZING PERI-OPERATIVE PATHWAYS CAN REDUCE LENGTH OF STAY AND HOSPITAL COSTS RELATED TO PANCREATICODUODENECTOMY PATIENTS W Conway, MD, J Bolton, MD, Ochsner Medical Center, New Orleans, US


TABLE OF CONTENTSPoster Listings

POSTER LISTINGS

★P007 NEOADJUVANT FOLFIRINOX IN BORDERLINE RESECTABLE PANCREATIC ADENOCARCINOMA Alessandro Paniccia, MD, Barish H Edil, MD, Richard D Schulick, MD, MBA, Csaba Gajdos, MD, Joshua T Byers, MS, Cheryl Meguid, DNP, ACNP, Martin D McCarter, MD, Department of General Surgery, University of Colorado, Denver, USA, Denver, US

★P008 PANCREATIC PENETRATION OF MEROPENEM AND DOSAGE CONSIDERATIONS BASED ON SITE-SPECIFIC PHARMACOKINETIC-PHARMACODYNAMIC ANALYSIS Naru Kondo, MD, Kazuro Ikawa, PhD, Yoshiaki Murakami, MD, Kenichiro Uemura, MD, Takeshi Sudo, MD, Yasushi Hashimoto, MD, Hiroki Ohge, MD, Norifumi Morikawa, PhD, Taijiro Sueda, MD, Department of Surgery, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, JP

★P009 RESCUE ERCP AND EMERGENCY PANCREATIC DUCT STENT PLACEMENT FOR THE MANAGEMENT OF POST-ERCP PANCREATITIS: RESULTS OF A LARGE CASE SERIES AT THE DISTRICT HOSPITAL IN JAPAN Hiroyuki Hisai, MD, PhD, Tasuku Hirako, MD, Yohei Arihara, MD, Yuuki Ikeda, MD, Yutaka Koshiba, MD, Etsu Miyazaki, MD, PhD, Department of Gastroenterology, Japan Red Cross Date General Hospital, Date, Japan, Date, JP

★P077 HIGH PHOSPHATE SERUM LEVELS CORRELATE WITH THE SEVERITY OF EXPERIMENTAL SEVERE ACUTE PANCREATITIS - INSIGHT INTO THE PURINERGIC SYSTEM Guilherme S Mazzini, MD, Daniel T Jost, Denise B Ramos, MS, Jean P Oses, PhD, Mateus A Zeni, Rafael Machoseki, Luiza W Kist, PhD, Mauricio R Boggo, PhD, Carla D Bonan, PhD, Maria I Edelweiss, MD, PhD, Marta M Duarte, MS, Luis V Portela, PhD, Alessandro B Osvaldt, MD, PhD, Diogo O Souza, MD, PhD, Universidade Federal do Rio Grande do Sul, Universidade Catolica de Pelotas, Instituto Nacional de Ciencia e Tecnologia Translacional em Medicina (INCT-TM), Pontificia Universidade Catolica do Rio Grande do Sul, Universidade Luterana do Brasil., Porto Alegre, BR

P010 TARGETED THERAPY OF THE HEDGEHOG EFFECTOR GLI IN PANCREATIC AND AMPULLARY CANCER Kim C Honselmann, MD, Moritz Pross, MD, Thomas Brabletz, MD, PhD, Tobias Keck, MD, Phd, Ulrich F Wellner, PhD, MD, Dirk Bausch, MD, PhD, Department of General, Visceral-, Thoracic- and Vascular Surgery, University of Luebeck, Germany &Clinic for General and Visceral Surgery, University Medical Center Freiburg, Germany, Luebeck, DE

P011 COMPOSITE ALTERATIONS IN GLYCOLYTIC METABOLISM AND AUTOPHAGY ARE ASSOCIATED WITH POOR PROGNOSIS IN PANCREATIC DUCTAL CARCINOMA A K Witkiewicz, MD, W B Wachsmann, MD, G H Baek, MD, J C Mansour, MD, Michael A Choti, MD, E S Knudsen, MD, Departments of 1Surgery and 2Pathology, University of Texas Southwestern Medical Center, Dallas, TX USA, Dallas, US

P012 THE EFFECT OF NEOADJUVANT CHEMORADIATION ON GENE EXPRESSION PATTERNS OF PANCREATIC ADENOCARCINOMA Andrew M Baschnagel, MD, Bryan J Thibodeau, PhD, Laura E Fortier, MS, Tim J Geddes, BS, Barbara L Pruetz, BS, Billie E Ketelsen, BS, Brandon M Stone, MD, George D Wilson, PhD, Robert P Jury, MD, William Beaumont Hospital, Royal Oak, US

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Poster Listings

POSTER LISTINGS

P013 HIGH-VOLUME SURGEONS: ARE THERE DIFFERENCES AMONG THE BUSIEST ONES? Prashant B Sukharamwala, MD, Sharona B Ross, MD, Amanda E Smart, Franka Co, BS, Carry E Ryan, MS, Thomas W Wood, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

P014 FROM THE OR TO THE MOUSE: WHAT INFLUENCES SUCCESSFUL PDX ENGRAFTMENT? Andrea Porpiglia, MD, Igor Astsaturov, MD, PHD, Vladimir Khazak, PhD, Harry S Cooper, MD, John P Hoffman, MD, Fox Chase Cancer Center, Philadelphia, US

P015 EXPRESSION OF B7-H5 IN NORMAL PANCREAS AND PANCREATIC CANCER Joshua T Byers, Yuwen Zhu, PhD, Alessandro Paniccia, MD, Nate W Kahn, PhD, Lieping Chen, MD, PhD, Richard D Schulick, MD, Barish H Edil, MD, Department of Surgery, University of Colorado, Denver, Colorado; Department of Immunology, Yale University, New Haven, Connecticut, Denver, US

P016 THE NEW FULLY AUTOMATED SYSTEM FOR KI67 EVALUATION IN PANCREATIC NEUROENDOCRINE TUMORS (PNET). WOULD IT BE POSSIBILE TO OBTAIN A STANDARD TO GRADE EVALUATION? Niccola Funel1,2, PhD, Piniccia Faviana1, MD, Luca E Pollina1, MD, Vittorio Perrone2, MD, Fabio Caniglia2, MD, Ugo Boggi2, MD, Fulvio Basolo1, MD, BSD, Daniela Campani1, MD, 1 Departement of Surgery, Division of Surgical Pathology, University of Pisa, Italy; 2 Department of Oncology, Division of General and transpant Surgery., Pisa, IT

P017 EVALUATING COMPARATIVE EFFECTIVENESS WITH OBSERVATIONAL DATA: ENDOSCOPIC ULTRASOUND AND SURVIVAL IN PANCREATIC CANCER Abhishek D Parmar, MD, Kristin M Sheffield, PhD, Yimei Han, MS, Gabriela M Vargas, MD, Praveen Guturu, MD, Yong-Fang Kuo, PhD, James S Goodwin, MD, Taylor S Riall, MD, PhD, UCSF-East Bay, University of Texas-Medical Branch, Galveston, US

P018 MINIMAL CLINICAL IMPACT OF DIAGNOSTIC ERRORS IN CYSTIC TUMORS OF THE PANCREAS Marco Del Chiaro, MD, PhD, Associate, Professor, Ralf Segersvard, MD, PhD, Ralf Segersvard, MD, PhD, Raffaella Pozzi Mucelli, MD, Elena Rangelova, MD, Nikolaos Kartalis, MD, PhD, Christoph Ansorge, MD, PhD, Urban Arnelo, MD, PhD, John Blomberg, MD, PhD, Matthias Lohr, MD, PhD, Professor, Caroline Verbeke, MD, PhD, Division of Surgery, Department of Clinical Science, Intervention and Technology (CLINTEC). Karolinska Institutet - Stockholm, Sweden, Stockholm, SE

P019 THE EFFECT OF PREOPERATIVE BILIARY DRAINAGE ON SURGICAL OUTCOME FOLLOWING PANCREATICODUODENECTOMY FOR PANCREAS HEAD CANCER Kenichiro Uemura, MD, Yoshiaki Murakami, MD, Kawai Kawai, MD, Ken-ichi Okada, MD, Ippei Matsumoto, MD, Sadaki Asari, MD, Sohei Satoi, MD, Hiroaki Yanagimoto, MD, Masayuki Sho, MD, Takahiro Akahori, MD, Goro Honda, MD, Masanao Kurata, MD, Fuyuhiko Motoi, MD, Michiaki Unno, MD, Multicenter Study Group of Pancreatobiliary Surgery (MSG-PBS), Hiroshima, JP



POSTER LISTINGS

P020 DETAILED ANALYSIS OF EMT AND TUMOR BUDDING IDENTIFIES PREDICTORS OF LONG TERM SURVIVAL IN PANCREATIC DUCTAL ADENOCARCINOMA Peter Bronsert, MD, Silvia Timme, MD, Ilona Kohler, MD, Martin Werner, Prof, Dirk Bausch, MD, Ulrich T Hopt, Prof, Tobias Keck, Prof, Ulrich F Wellner, MD, Clinic for Surgery UKSH Campus Lubeck, Institute of Pathology University Medical Center Freiburg, Lubeck, DE

P021 WHO TRAVELS FOR CANCER CARE? REGIONALIZATION OF PANCREATECTOMY IN MASSACHUSETTS Lindsay A Bliss*, MD, Theodore P McDade**, MD, Zeling Chau**, MD, MPH, Jillian K Smith**, MD, Catherine J Yang*, MD, Sing Chau Ng*, MS, Bruce B Cohen***, PhD, Giles F Whalen**, MD, Mark P Callery*, MD, Jennifer F Tseng*, MD, MPH, *Department of Surgery, Beth Israel Deaconess Medical Center; **Department of Surgery, UMass Memorial Medical Center; ***Center for Health Information, Statistics, Research, and Evaluation, Massachusetts Department of Public Health, Boston, US

P022 SINGLE-INSTITUTION EXPERIENCE WITH RESECTION OF SIDE-BRANCH IPMN: A REVIEW OF PRE-OPERATIVE CHARACTERISTICS AND FINAL PATHOLOGIC DIAGNOSIS John Dortch, MD, Michael Antiporda, MD, John A Stauffer, MD, Horacio J Asbun, MD, Mayo Clinic- Florida, Jacksonville, US

P023 DOES ROUTINE DRAINAGE OF THE OPERATIVE BED FOLLOWING ELECTIVE DISTAL PANCREATECTOMY REDUCE COMPLICATIONS? - AN ANALYSIS OF THE ACS-NSQIP PANCREATECTOMY DEMONSTRATION PROJECT Stephen W Behrman, MD, Ben Zarzaur, MD, Abhishek Parmer, MD, Taylor Riall, MD, Bruce Hall, MD, Henry Pitt, MD, University of Tennessee Health Science Center, Memphis, US

P024 STRONG MEMBRANOUS EXPRESSION OF PLECTIN IS AN INDEPENDENT PREDICTOR OF IMPROVED SURVIVAL AFTER RESECTION OF PANCREATIC HEAD DUCTAL ADENOCARCINOMA Moritz Pross, MD, Peter Bronsert, MD, Martin Werner, Prof, Silvia Timme, MD, Frank Makowiec, Ulrich Hopt, Prof, Dirk Bausch, MD, Tobias Keck, Prof, Ulrich F Wellner, MD, Clinic for Surgery, UKSH Campus Lubeck, Germany; Institute of Pathology, University Medical Center Freiburg, Germany, Lubeck, DE

P025 IMPACT OF PANCREATIC FISTULA ON RECURRENCE AND LONG-TERM PROGNOSIS OF PERIAMPULLARY ADENOCARCINOMAS AFTER PANCREATICODUODENECTOMY Dowan Kim, BSc, Pablo E Serrano, MD, MPH, MSc, Peter T Kim, MD, Paul D Greig, MD, Carol-Anne Moulton, MD, PhD, Steven Gallinger, MD, MSc, Alice C Wei, MD, CM, MSc, Sean P Cleary, MD, MPH, MSc, Department Of Surgery, Toronto General Hospital,Toronto,ON, Windsor, CA

P026 A NOVEL APPROACH TO PATIENT EDUCATION: THE ICAREBOOK FOR PANCREATIC CANCER Christopher L Wolfgang, MD, PhD, Toby Cornish, MD, PhD, Michael Erdek, Kyoung ran Eun, Na’im K Fanaian, MD, Elliot K Fishman, MD, Joseph M Herman, Daniel Laheru, MD, Joanna K Law, MD, Anne Marie Lennon, MD, Corinne Sandone, Ralph H Hruban, MD, Departments of Pathology, Oncology, Surgery, Radiation Oncology, Radiology, Gastroenterology, Anesthesia and 8Art As Applied To Medicine; Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University, Baltimore, MD, Baltimore, US

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Poster Listings

POSTER LISTINGS

P027 MODIFIED RADICAL ANTEGRADE MODULAR PANCREATOSPLENECTOMY FOR ADENOCARCINOMA OF THE LEFT PANCREAS-SIGNIFICANCE OF EN BLOC RESECTION INCLUDING THE ANTERIOR RENAL FASCIA Hirohisa Kitagawa, MD, Hidehiro Tajima, MD, Hisatoshi Nakagawara, MD, Isamu Makino, MD, Tomoharu Miyashita, MD, Hirofumi Terakawa, MD, Shinichi Nakanuma, MD, Masatoshi Shouji, MD, Hironori Hayashi, MD, Hiroyuki Takamura, MD, Tetsuo Ohta, MD, Kanazawa University, Kanazawa, JP

P028 IDENTIFICATION OF RESECTION FOR BRANCH DUCT TYPE IPMN Seiko Hirono, MD, Masaji Tani, MD, Manabu Kawai, MD, Ken-ichi Okada, MD, Motoki Miyazawa, Atsushi Shimizu, MD, Yuji Kitahata, Hiroki Yamaue, Wakayama Medical University, Wakayama, JP

P029 ROBOTIC ASSISTED PANCREATICODUODENECTOMY MAY BE ASSOCIATED WITH AN INCREASED LIKELIHOOD OF RECEIVING ADJUVANT CHEMOTHERAPY M Khreiss, MD, Murtaza Shakir, MD, Brian Boone, MD, Mazen Zenati, MD, PHD, David Bartlett, MD, Amer Zureikat, MD, Herbert Zeh III, MD, Melissa Hogg, MD, University of Pittsburgh Medical Center, Pittsburgh, US

P030 LEARNING CURVE FOR ROBOTIC DISTAL PANCREATECTOMY M Shakir, MD, M Khreiss, MD, P M Polanco, MD, B A Boone, MD, M Zenati, MPH, M Hogg, MD, H Zeh, MD, A H Zureikat, MD, University of Pittsburgh Medical Center, Pittsburgh, US

P031 COMPARISON OF TUMOR MARKERS FOR PREDICTING NON-FUNCTIONING PANCREATIC NEUROENDOCRINE TUMOR OUTCOME Jovenel Cherenfant, MD, Susan J Stocker, Mistry K Gage, MS, Brittany Lapin, MS, Edward Wang, PhD, Jonathan C Silverstein, MD, Kathy Mangold, PhD, Tiffany A Thurow, MD, Melanie Odeleye, MD, Karen L Kaul, MD, Curtis R Hall, MD, Ihab Lamzabi, MD, Paolo Gattuso, MD, David J Winchester, MD, Robert W Marsh, MD, Kevin K Roggin, MD, David J Bentrem, MD, Marshall S Baker, MD, Mark S Talamonti, MD, Richard A Prinz, MD, NorthShore University HealthSystems, Evanston, IL, Jesse Brown Medical Center, Chicago, IL, University of Chicago, Chicago, IL, Rush University Medical Center, Chicago, IL, Munster, US

P032 PREDICTING AGGRESSIVE BEHAVIOR IN NON-FUNCTIONING PANCREATIC NEUROENDOCRINE TUMORS Jovenel Cherenfant, MD, Susan J Stocker, Mistry K Gage, MS, Hongyan Du, MS, Tiffany A Thurrow, MD, Melanie Odeleye, MD, Scott Schimpke, MD, Karen L Kaul, MD, Curtis R Hall, MD, Ihab Lamzabi, MD, Paolo Gattuso, MD, David J Winchester, MD, Robert W Marsh, MD, Kevin K Roggin, MD, David J Bentrem, MD, Marshall S Baker, MD, Richard A Prinz, MD, Mark S Talamonti, MD, NorthShore University HealthSystems, Evanston, IL, Northwestern Finberg School of Medicine, Chicago, IL, Jesse Brown Medical Center, Chicago, IL, University of Chicago, Chicago, IL, Rush University Medical Center, Chicago, IL, Munster, US

P033 SOCIOECONOMIC STATUS AND SURGICAL OUTCOMES AFTER REGIONAL PANCREATECTOMY Heidi Schmidt, MD, Nakul Valsangkar, MD, Molly E Kilbane, Alexandra P Turner, MD, Michael G House, MD, Nicholas J Zyromski, MD, Attila Nakeeb, MD, C. Max Schmidt, MD, Eugene P Ceppa, MD, Indiana University School of Medicine, Department of Surgery, Indianapolis, US



POSTER LISTINGS

P034 RISK FACTORS FOR PANCREATIC FISTULA AFTER ROBOTIC PANCREATICODUODENECTOMY Patricio M Polanco, MD, Melissa E Hogg, MD, Murtaza Shakir, MD, Mazen S Zenati, MD, M.Haroon Choudry, MD, Brian A Boone, MD, Bartlett L David, MD, Herbert J Zeh, MD, Amer H Zureikat, MD, University of Pittsburgh Medical Center, Pittsburgh, US

P035 FIRST REPORT OF A PROSPECTIVE TRIAL OF PROTON THERAPY AND CONCOMITTANT CAPECITABINE FOR PATIENTS WITH NON METASTATIC UNRESECTABLE PANCREATIC ADENOCARCINOMA Romaine C Nichols, MD, Christopher G Morris, MS, Thomas J George, MD, Robert A Zaiden, MD, Elizabeth Johnson, MD, Bestoun H Ahmed, MD, Meng Wei Ho, PhD, Soon N Huh, PhD, Nancy P Mendenhall, MD, Bradford S Hoppe, MD, University of Florida Proton Therapy Institute, Jacksonville, Florida, Jacksonville, US

P036 PORTAL VENOUS RESECTION IN CANCER OF THE PANCREATIC HEAD: WHAT ARE THE RELEVANT PREDICTORS OF SURVIVAL? Hryhoriy Lapshyn, PhD, Ulrich Wellner, PhD, Birte Kulemann, PhD, Jens Hoeppner, PhD, Frank Makowiec, Prof, Peter Bronsert, PhD, Dirk Bausch, PhD, Tobias Keck, Prof, Ulrich Hopt, Prof, Uwe Wittel, PhD, Clinic for General and Visceral Surgery, University of Freiburg Medical Center, Germany. Department of Surgery, University Hospital of Schleswig-Holstein Campus Lubeck, Germany. Institute of Clinical Pathology, University of Freiburg. Germany., Freiburg Im Br., DE

P037 THE CHANGING SPECTRUM OF SURGICALLY TREATED CYSTIC NEOPLASMS OF THE PANCREAS Jennifer K Plichta, MD, MS, Jacqueline A Brosius, BS, Sam Pappas, MD, Gerard J Abood, MD, MS, Gerard V Aranha, MD, Loyola University Medical Center, Maywood, US

P038 SHOULD ALL BRANCH-DUCT IPMN’S BE RESECTED? Jennifer K Plichta, MD, MS, Zachary Fridirici, MD, Anjali S Godambe, DO, Sherri Yong, MD, Sam Pappas, MD, Gerard J Abood, MD, MS, Gerard V Aranha, MD, Loyola University Medical Center, Maywood, US

P039 COMPARISON OF ROBOTIC VERSUS OPEN PANCREATICODUODENECTOMY Brian A Boone, MD, Stephanie Downs-Canner, MD, Jennifer Steve, BS, Mazen S Zenati, MD, PhD, Melissa E Hogg, MD, A. James Moser, MD, David L Bartlett, MD, Haroon A Choudry, MD, Herbert J Zeh, MD, Amer H Zureikat, MD, University of Pittsburgh; Beth Israel Deaconess, Pittsburgh, US

P040 TRENDS IN THE USE OF PRE-OPERATIVE RADIATION FOR ADENOCARCINOMA OF THE PANCREAS IN THE UNITED STATES Erin E Burke, MD, Resident, Schelomo Marmor, PhD, Pamela Portschy, MD, Resident, Beth A Virnig, PhD, Todd M Tuttle, MD, MS, Eric H Jensen, MD, University of Minnesota, Minneapolis, US

P041 INCREASED NUMBER OF PERINEURAL INVASION IS INDEPENDENTLY ASSOCIATED WITH POOR SURVIVAL OF PATIENTS WITH RESECTABLE PANCREATIC CANCER Naru Kondo, MD, Yoshiaki Murakami, MD, Kenichiro Uemura, MD, Takeshi Sudo, Yasushi Hashimoto, MD, Hayato Sasaki, MD, Taijiro Sueda, MD, Institute of Biomedical and Health Sciences Applied Life Sciences Surgery, Hiroshima University, Hiroshima, JP

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POSTER LISTINGS

P042 DOES PANCREATIC INTRAEPITHELIAL NEOPLASIA PREDICT RECURRENCE OF PANCREATIC ADENOCARCINOMA OR DEVELOPMENT OF A SECOND PRIMARY IN THE REMNANT GLAND? Trang K Nguyen, MD, Jennifer Steve, Amer H Zureikat, MD, Aatur D Singhi, MD, Herbert J Zeh, MD, University of Pittsburgh Medical Center, Pittsburgh, US

P043 IRREVERSIBLE ELECTROPORATION IS SAFE AND FEASABLE FOR THE CONTROL AND TREATMENT OF LOCALLY-ADVANCED AND BORDERLINE-RESECTABLE PANCREATIC CANCER: SHORT TERM RESULTS Megan Winner, MD, Irene Epelboym, MD, Michael D Kluger, MD, John A Chabot, MD, Columbia University Medical Center New York Presbyterian Hospital, New York, US

P044 IS ROUX-Y BINDING PANCREATICO-JEJUNAL ANASTOMOSIS (BPJA) FEASIBLE FOR PATIENTS UNDERGOING DISTAL PANCREATECTOMY? Anne Antila, MD, Juhani Sand, MD, PhD, Sari Raty, MD, PhD, Isto Nordback, MD, PhD, Johanna Laukkarinen, MD, PhD, Dept. of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland., Tampere, FI

P045 LENGTH OF STAY AFTER PANCREATICODUODENECTOMY: WHAT IS THE GOAL? Thomas W Wood, MD, Sharona B Ross, MD, Amanda E Smart, Diana Fisler, Carrie E Ryan, MS, Paul G Toomey, MD, Kenneth Luberice, BS, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

P046 PATENCY RATES OF PORTAL VEIN/SUPERIOR MESENTERIC VEIN RECONSTRUCTION AFTER PANCREATECTOMY FOR PANCREATIC ADENOCARCINOMA A N Krepline, K Duelge, K K Christians, B George, P S Ritch, B A Erickson, J P Thomas, A Mahmoud, E J Quebbeman, K K Turaga, F M Johnston, T C Gamblin, D B Evans, S Tsai, Medical College of Wisconsin, Milwaukee, US

P047 PROPHYLACTIC ANTICOAGULATION FOR SUPERIOR MESENTERIC VEIN (SMV) OR PORTAL VEIN (PV) NARROWING/OCCLUSION IN BORDERLINE RESECTABLE (BLR) PANCREATIC ADENOCARCINOMA (PC) PATIENTS A N Krepline, K Duelge, B George, P S Ritch, B A Erickson, J P Thomas, A Mahmoud, E J Quebbeman, K K Turaga, F M Johnston, T C Gamblin, K K Christians, D B Evans, S Tsai, Medical College of Wisconsin, Milwaukee, US

P048 CLINICAL OUTCOMES IN PANCREATIC ADENOCARCINOMA ASSOCIATED WITH BRCA2 MUTATION Ojas H Vyas, MD, Keith Leung, MD, Wasif M Saif, MD, MBBS, Tufts University School of Medicine, Tufts Cancer Center, Boston, US

P049 STEREOTACTIC BODY RADIATION THERAPY FOR PANCREATIC CANCER: THE JOHNS HOPKINS EXPERIENCE Shalini Moningi, BA, Siva P Raman, MD, Avani S Dholakia, BS, Amy Hacker-Prietz, MS, Timothy M Pawlik, MD, PhD, Lei Zheng, MD, Matthew J Weiss, MD, Daniel A Laheru, MD, Christopher L Wolfgang, MD, PhD, Joseph M Herman, MD, Msc, Johns Hopkins Hospital, Baltimore, US

P050 INVASIVE IPMN: TWO DISTINCT PATTERNS OF MICROSCOPIC INVASION WITH DIFFERENT BIOLOGY Jason F Solus, MD, Ladan Fazlollahi, MD, MPH, Carlos Fernandez-Del Castillo, MD, Giovanni Marchegiani, MD, Martha B Pitman, MD, Mari Mino-Kenudson, MD, Massachusetts General Hospital, Boston, US



POSTER LISTINGS

P051 PRE-SBRT METABOLIC TUMOR VOLUME AND TOTAL LESION GLYCOLYSIS PREDICT IMPROVED SURVIVAL IN PATIENTS WITH LOCALLY ADVANCED PANCREATIC CANCER RECEIVING STEREOTACTIC BODY RADIATION THERAPY Avani S Dholakia, BS, Muhammad Chaudhry, MD, Daniel T Chang, MD, Jeffrey P Leal, BA, Amy Hacker-Prietz, PAC, Zheng Su, Matthew J Weiss, MD, Katherine E Oteiza, MS, Mary E Griffith, BSN, Richard L Wahl, MD, Erik Tryggestad, PhD, Timothy Pawlik, MD, MBA, Daniel A Laheru, MD, Christopher L Wolfgang, MD, PhD, Albert C Koong, MD, PhD, Joseph M Herman, MD, MSc, Johns Hopkins Universtiy School of Medicine and Stanford University School of Medicine, Baltimore, US

P052 WITHDRAW P053 FINANCIAL BENEFITS OF A HEPATOPANCREATICOBILIARY PROGRAM Sharona B Ross, MD, Richard L Klein, Carrie E Ryan, MS, Thomas W Wodd, MD, Prashant B Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

P054 HIGH-VOLUME HOSPITALS WITH HIGH AND LOW VOLUME SURGEONS: IS THERE A ‘FIELD EFFECT FOR PANCREATICODUODENECTOMY? Thomas W Wood, MD, Sharona B Ross, MD, Amanda E Smart, Carrie E Ryan, MS, Prashant B Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

P055 WITHDRAW P056 COST-EFFECTIVENESS AFTER PANCREATICODUODENECTOMY: BOLSTERING THE VOLUME ARGUMENT Jeffrey M Sutton, MD, Gregory C Wilson, MD, Koffi Wima, MS, Dennis J Hanseman, PhD, Ralph C Quillin III, MD, Ian M Paquette, MD, Jeffrey J Sussman, MD, Michael J Edwards, MD, Syed A Ahmad, MD, Shimul A Shah, MD, Daniel E Abbott, MD, Cincinnati Clinical Research Group in Surgery, Department of Surgery, University of Cincinnati Medical Center, Cincinnati, OH, Cincinnati, US

P057 PANCREATICODUODENECTOMY FOR PANCREATIC CANCER: IS THERE A SURVIVAL DIFFERENCE FOR PLANNED VERSUS UNPLANNED PORTAL VEIN RESECTION? Yasushi Hashimoto, MD, Yoshiaki Murakami, MD, Kenichiro Uemura, MD, Takeshi Sudo, MD, Naru Kondo, MD, Sasaki Hayato, MD, Ohge Hiroki, MD, Taijiro Sueda, MD, Department of Surgery, Division of Clinical Medical Science, Programs for Applied Biomedicine, Hiroshima University, Hiroshima, JP

P058 PERIOPERATIVE AND LONG TERM OUTCOME AFTER EXTENDED (PORTAL VEIN, MULTIVISCERAL) RESECTION FOR CANCER OF THE PANCREATIC HEAD Birte Kulemann, MD, Uwe Wittel, MD, Ulrich F Wellner, MD, Tobias Keck, MD, Peter Bronsert, MD, Ulrich T Hopt, MD, Jens Hoeppner, MD, Frank Makowiec, MD, Department of Genral &Visceral Surgery, Department of Pathology, University Hosptial Freiburg, Freiburg, Germany, Freiburg, GE

P059 CT SIGNS SUGGESTING MALIGNANCY IN BRANCH DUCT TYPE IPMNS Carla Cappelli, PhD, Rosa Cervelli, MD, Salvatore Mazzeo, MD, Mario Belluomini, MD, Daniela Campani, MD, Ugo Boggi, MD, Carlo Bartolozzi, MD, Diagnostic and Interventional Radiology-University of Pisa, Pisa, IT

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POSTER LISTINGS

P060 IS ANTACID THERAPY AFTER PANCREATODUODENECTOMY NECESSARY? CONTEMPORARY GLOBAL PRACTICE OF PANCREATIC SURGEONS James R Butler, MD, Eugene P Ceppa, MD, Michael G House, MD, Attila Nakeeb, MD, C. M Schmidt, MD, Phd, Nicholas J Zyromski, MD, Department of Surgery, Indiana University School of Medicine, Indianapolis, US

P061 EFFECTS OF GEMCITABINE AND STEREOTACTIC BODY RADIOTHERAPY ON QUALITY OF LIFE IN LOCALLY ADVANCED PANCREATIC CANCER Avani S Dholakia, BS, Daniel T Chang, MD, Karyn A Goodman, MD, Elizabeth Sugar, PhD, Amy Hacker-Prietz, PAC, Laurie Ann Columbo, BSN, Mary E Griffith, BSN, Aaron T Wild, BA, Timothy M Pawlik, MD, MBA, George A Fisher, MD, PhD, Susannah Ellsworth, MD, Albert Koong, MD, PhD, Joseph M Herman, MD, MSc, Johns Hopkins Universtiy School of Medicine, Stanford University School of Medicine, and Memorial Sloan Kettering Cancer Center, Baltimore, US

P062 FEASIBILITY OF RESECTION AFTER INDUCTION THERAPY FOR LOCALLY ADVANCED PANCREATIC CANCER A Amini, MD, A N Krepline, BS, A Mahmoud, BS, K Duelge, BS, B George, MD, P S Ritch, MD, B A Erickson, MD, K K Christians, MD, D B Evans, MD, S Tsai, MD, Medical College of Wisconsin, Milwaukee, US

P063 PROGNOSTIC IMPACT OF SINGLE LYMPH NODE STATIONS IN RESECTED PANCREATIC HEAD CANCER Giuseppe Malleo, MD, Laura Maggino, MD, Francesco Gulino, Md, Eleonora Morelli, MD, Giovanni Butturini, PhD, Claudio Bassi, MD, Roberto Salvia, PhD, Unit of Surgery B, The Pancreas Institute, University of Verona Hospital Trust; Unit of Pathology, The Pancreas Institute University of Verona Hospital Trust, Verona, IT

P064 PERIOPERATIVE RISK FACTORS FOR DELAYED GASTRIC EMPTYING FOLLOWING PANCREATICODUODENECTOMY Jamie Robinson, MD, Paula Marincola, BA, Julia Shelton, MD, MPH, Kamran Idrees, MD, Nipun Merchant, MD, Alexander Parikh, MD, MPH, Vanderbilt University Medical Center, Nashville, US

P065 INCIDENCE OF ADDITIONAL PRIMARY MALIGNANCIES IN PATIENTS WITH PANCREATIC NEUROENDOCRINE TUMORS AND CARCINOID Jamie Robinson, MD, Rondi Kauffmann, MD, MPH, Li Wang, MS, Sharon Phillips, MS, Kamran Idrees, MD, Nipun Merchant, MD, Alexander Parikh, MD, MPH, Vanderbilt University Medical Center, Nashville, US

P066 LAPAROSCOPIC PANCREATICOJEJUNAL ANASTOMOSIS DURING TOTAL LAPAROSCOPIC PANCREATICODUODENECTOMY FOR PANCREATIC CANCER: IS THERE A TEHNIQAL PREFERENCE? Igor E Khatkov - 1,2, Professor, MD, PhD, Victor V Tsvirkun - 1, Professor, MD, PhD, Roman E Izrailov - 1,2, Professor, MD, PhD, Pavel S Tyutyunnik, MD, 1 - Moscow Scientific Research Institute of Gastroenterology; 2 - Moscow State University of Medicine and Dentistry, Moscow, RU

P067 THE SAFETY AND EFFICACY OF PANCREATIC DUCT STENT PLACEMENT IN THE EMERGENCY ERCP OF ACUTE BILIARY PANCREATITIS Hiroyuki Hisai, MD, PhD, Tasuku Hirako, MD, Yohei Arihara, MD, Yuuki Ikeda, MD, Yutaka Koshiba, MD, Etsu Miyazaki, MD, PhD, Department of Gastroenterology, Japan Red Cross Date General Hospital, Date, Japan, Date, JP



POSTER LISTINGS

P068 FEASIBILITY AND OUTCOMES OF ROBOTICS IN THE SURGICAL MANAGEMENT OF PANCREATIC NECROSIS AND PSEUDOCYSTS Ramanathan M Seshadri, MD, Ryan Z Swan, MD, David Sindram, MD, PhD, David A Iannitti, MD, John B Martinie, MD, Carolinas Medical Center, Charlotte, US

SATURDAY, MAY 3, 2014★P069 QUANTIFYING THE BURDEN OF PERIOPERATIVE COMPLICATIONS FOLLOWING TOTAL PANCREATECTOMY USING THE POSTOPERATIVE MORBIDITY INDEX: A MULTI-INSTITUTIONAL PERSPECTIVE Jashodeep Datta, MD, Russell S Lewis Jr., BA, Steven M Strasberg, MD, Bruce L Hall, MD, Charles M Vollmer Jr, MD, The PMI Study Group, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA; Washington University School of Medicine, St. Louis, MO, Philadelphia, US

★P070 BRAUN ENTEROENTEROSTOMY AFFECTS DELAYED GASTRIC EMPTYING AFTER PYLORUS-PRESERVING PANCREATODUODENECTOMY: A RETROSPECTIVE REVIEW Yusuke Watanabe, MD, Takao Ohtsuka, MD, PhD, Hideyo Kimura, MD, Taketo Matsunaga, MD, Koji Tamura, MD, Noboru Ideno, MD, Teppei Aso, MD, Yoshihiro Miyasaka, MD, PhD, Junji Ueda, MD, PhD, Shunichi Takahata, MD, PhD, Masao Tanaka, MD, PhD, FACS, Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan, Fukuoka, JP

★P071 SINGLE INSTITUTION EXPERIENCE WITH NEOADJUVANT TREATMENT OF BORDERLINE RESECTABLE PANCREATIC ADENOCARCINOMA: ACHIEVING R0 RESECTION WITH MODERN CHEMOTHERAPY Nathan Bolton, MD, William Conway, MD, John Bolton, MD, Ochsner Clinic Foundation, New Orleans, US

★P072 A MULTIDISCIPLINARY CLINIC FOR PANCREATIC CANCER IMPROVES UTILIZATION OF THERAPY Suzanne C Schiffman, MD, Yongli Shuai, PhD, Ying Ding, PhD, Cindy Valko, Sharon Winters, David L Bartlett, MD, Amer H Zureikat, MD, Herbert J Zeh, MD, Melissa E Hogg, MD, University of Pittsburgh Medical Center, Pittsburgh, US

★P073 PANCREATICODUODENECTOMY WITH MAJOR VASCULAR RESECTION: A COMPARISON OF LAPAROSCOPIC VERSUS OPEN APPROACHES Kristopher P Croome, MD, MS, Michael B Farnell, MD, Mark J Truty, MD, Kaye Reid-Lombardo, MD, Florencia G Que, MD, David M Nagorney, MD, Michael L Kendrick, MD, Mayo Clinic, Rochester, US

★P074 READMISSION AFTER PANCREATICODUODENECTOMY: THE INFLUENCE OF THE VOLUME EFFECT BEYOND MORTALITY Jeffrey M Sutton, MD, Gregory C Wilson, MD, Koffi Wima, MS, Ralph C Quillin III, MD, Dennis J Hanseman, PhD, Ian M Paquette, MD, Jeffrey J Sussman, MD, Syed A Ahmad, MD, Shimul A Shah, MD, Daniel E Abbott, MD, Cincinnati Clinical Research Group in Surgery, Department of Surgery, University of Cincinnati Medical Center, Cincinnati, OH, Cincinnati, US

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POSTER LISTINGS

★P075 COHORT STUDY OF THE INCIDENCE OF EXTRAPANCREATIC NEOPLASMS DURING CLINICAL AND RADIOLOGIC SURVEILLANCE OF PATIENTS WITH BRANCH-DUCT IPMN Giuseppe Malleo, MD, Giovanni Marchegiani, MD, Alex Borin, MD, Federico Accordini, Md, Claudio Bassi, MD, Roberto Salvia, Unit of Surgery B, The Pancreas Institute, University of Verona Hospital Trust, Verona, IT

★P076 OPERATIVE MORTALITY AFTER MAJOR PANCREATIC CANCER SURGERY IN NEW YORK STATE - HAS A REGIONALIZATION MADE A DIFFERENCE? A 10-YEAR ANALYSIS Pragatheeshwar Thirunavukarasu, MD, Chetasi Talati, MD, Kristopher Attwood, Boris W Kuvshinoff, MD, Roswell Park Cancer Institute, Buffalo, US

★P077 Moved to Friday, May 2 viewing (see page 21 for details)

★P078 LONG-TERM OUTCOMES FAVOR PYLORUS PRESERVING PANCREATICODUODENECTOMY OVER DUODENUM PRESERVING PANCREATIC HEAD RESECTION FOR CHRONIC PANCREATITS: A META-ANALYSIS AND SYSTEMATIC REVIEW Prashant B Sukharamwala, MD, Sharona B Ross, MD, S Parikh, Carrie E Ryan, MS, Thomas W Wood, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

P079 A COMPLEX CASE OF PANCREATIC DUCTAL ADENOCARCINOMA FORMING TWO MASS LESIONS: MOLECULAR AND FUNCTIONAL ANALYSIS A K Witkiewicz, MD, R Kittler, PhD, J C Mansour, MD, E S Knudsen, MD, M A Choti, MD, Departments of Surgery and Pathology, University of Texas Southwestern Medical Center, Dallas, TX USA, Dallas, US

P080 REDUCTION OF DEOXYCYTIDINE KINASE(DCK) PROTEIN EXPRESSION LEVEL AND ENZYME ACTIVITY WERE CAUSE OF GEMCITABINE ACQUIRED RESISTANCE IN PANCREATIC CANCER CELLS Kei Kawaguchi, PhD, Fuyuhiko Motoi, PhD, Shinichi Egawa, PhD, Michiaki Unno, PhD, Division of Hepato-Bilialy Pancreatic Surgery, Department of Surgery, Tohoku University Hospital, Sendai, Miyagi, JP

P081 REPEATED NON-INVASIVE RADIOFREQUENCY TREATMENT OF PANCREATIC CANCER CELLS DEMONSTRATES SUSTAINED EFFECTIVENESS AND IMPROVED SUPPRESSION OF CANCER CELL PROLIFERATION Hop S Tran Cao, MD, Warna D Kaluarachchi, MS, Jonathan C Vo, BS, Douglas C Huynh, BS, Steven A Curley, MD, Department of Surgical Oncology, U.T. MD Anderson Cancer Center, Houston, TX; University of Texas Health Science Center at Houston Medical School, Houston, TX, Houston, US

P082 OXALIPLATIN AND 5-FU UPREGULATE B7-H1 EXPRESSION IN HUMAN PANCREATIC CANCER CELL LINES Alessandro Paniccia, MD, Yuwen Zhu, PhD, Joshua T Byers, MS, Nate W Kahn, PhD, Sanjana Mehrotra, MD, Richard D Schulick, MD, MBA, Barish H Edil, MD, Department of General Surgery, University of Colorado, Denver, Colorado, USA, Denver, US



POSTER LISTINGS

P083 GEMCITABINE- UKRAIN COMBINATION TREATMENT MODULATES MMP9 EXPRESSION IN PRIMARY PANCREATIC ADENOCARCINOMA CELL CULTURES Lucia Botta1, MSD, Maria Denaro1, BSD, Alessandra Alvino1, BSD, Claudio Ricci1, PhD, Luca E Pollina1, MD, Fabio Caniglia2, MD, Nelide De Lio2, MD, Ugo Boggi2, MD, Daniela Campani1, MD, Niccola Funel1,2, PhD, 1 Department of Surgery, Division of Surgical Pathology, University of Pisa, Italy; 2 Department of Oncology, Division of General and transplant Surgery, University of Pisa, Italy, Pisa, IT

P084 IL-35 PROMOTES PANCREAS CANCER GROWTH THROUGH ENHANCEMENT OF PROLIFERATION AND INHIBITION OF APOPTOSIS Michael B Nicholl, MD, Chelsea L Ledgerwood, BS, Xuhui Chen, MD, Alberto Diaz-Arias, MD, Yujiang Fang, MD, PhD, Qian Bai, BA, Chenglu Qin, MD, University of Missouri, Columbia, US

P085 SURGERY AS AN UNDERUTILIZED TREATMENT MODALITY IN PATIENTS WITH LOCALIZED PANCREATIC CANCER - A NATIONAL ANALYSIS OF TRENDS AND OUTCOMES Madeleine Strohl, BA, Siavash Raigani, BA, John Ammori, MD, Jeffrey Hardarce, MD, Julian Kim, MD, Case Western Reserve University School of Medicine, Division of Surgical Oncology University Hospital Case Medical Center, Cleveland, OH, Shaker Heights, US

P086 THE RIGHT HEPATIC ARTERY FROM THE GASTRODUODENAL ARTERY AT PANCREATODUODENECTOMY Disi Hao, Dongzhu Mao, Heilongjiang Provincial Hospital, Harbin, CN

P087 AN ORGANIC IMPEDIMENT MIGHT BE ONE OF RISK FACTOR OF DELAYED GASTRIC EMPTYING AFTER PYLORUS PRESERVING PANCREATICODUODENECTOMY Hisashi Kosaka, MDPhD, Nobukazu Kuroda, Kazuhiro Suzumura, Yugo Uda, Seikan Hai, Yuichi Kondo, Syogo Tanaka, Ikuo Nakamura, Yasukane Asano, Toshihiro Okada, Tadamichi Hirano, Yuji Iimuro, Jiro Fujimoto, Hyogo College of Medicine, Dept of Surgery, Nishinomiya, JP

P088 A CASE REPORT OF DISTAL PANCREATECTOMY WITH EN BLOCK CELIAC AXIS RESECTION (DP-CAR) WITHOUT PREOPERATIVE INTERVENTIONAL ARTERIAL EMBOLISM FOR PANCREATIC BODY CANCER INVADED TO CELIAC AXIS WITH REPLACED RIGHT HEPATIC ARTERY Toshiyuki Moriya, MD, PhD, Koichiro Ozawa, MD, PhD, Shigeo Hasegawa, MD, PhD, Masaomi Mizutani, MD, PhD, Takayuki Higashi, MD, Yukinori Kamio, MD, PhD, Moriyoshi Yokoyama, MD, Ai Takahashi, MD, Satoshi Takai, MD, Osamu Usuba, MD, PhD, Okitama general hospital, Kawanishi-machi, JP

P089 LAPAROSCOPIC PYLORUS-PRESERVING PANCREATODUODENECTOMY WITH DOUBLE JEJUNAL LOOP RECONSTRUCTION. INITIAL EXPERIENCE WITH 12 CASES Marcel Machado, MD, Fabio Makdissi, MD, Rodrigo Surjan, MD, Marcel C Machado, MD, university of sao paulo, Sao Paulo, BR

P090 SINGLE PORT LAPAROSCOPIC DISTAL PANCREATECTOMY. INITIAL EXPERIENCE WITH 14 CASES Marcel A Machado, MD, Fabio Makdissi, MD, Rodrigo Surjan, MD, Marcel C Machado, university of sao paulo, Sao Paulo, BR

P091 SAFE TECHNIQUE FOR DISTAL PANCREAS RESECTION WITH POLYSORB CLIP IN THE VIEW OF 150 CASES Gyula Farkas Jr., PhD, Gyula Farkas, DSc, Gyorgy Lazar, DSc, University of Szeged Department of Surgery, Szeged, HU

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POSTER LISTINGS

P092 THE IMPACT OF PRESERVATION OF THE LEFT GASTRIC ARTERY IN DISTAL PANCREATECTOMY WITH CELIAC AXIS EN-BLOC RESECTION (DP-CAR): PROPOSAL OF A NOVEL SURGICAL TECHNIQUE TO REDUCE DELAYED GASTRIC EMPTYING Hiroki Yamaue, MD, Manabu Kawai, MD, Ken-ichi Okada, MD, Masaji Tani, MD, Seiko Hirono, MD, Motoki Miyazawa, MD, Atsushi Shimizu, MD, Yuji Kitahata, MD, Second Department of Surgery, Wakayama Medical University, Japan, Wakayama, JP

P093 PROGNOSTIC SIGNIFICANCE OF ZEB1 IN STROMAL AND CANCER CELLS IN PANCREATIC HEAD CANCER Peter Bronsert, MD, Dirk Bausch, MD, Silvia Timme, MD, Martin Werner, Prof, Ulrich T Hopt, Prof, Tobias Keck, Prof, Ulrich F Wellner, MD, Clinic for Surgery UKSH Campus Lubeck, Institute of Pathology University Medical Center Freiburg, Lubeck, DE

P094 HOSPITAL READMISSION AFTER PANCREATICODUODENECTOMY IN A HIGH VOLUME CENTER J. Bart Rose, MD, Flavio Rocha, MD, Adnan Alseidi, MD, Thomas Biehl, MD, Farzad Alemi, MD, Scott Helton, MD, Virginia Mason Medical Center, Seattle, US

P095 SHORT TERM OUTCOMES OF THE WHIPPLE AT THE SPLENIC ARTERY (WATSA) PROCEDURE Major K Lee, IV, MD, PhD, Roheena Z Panni, MD, William G Hawkins, MD, Ryan C Fields, MD, David C Linehan, MD, Steven M Strasberg, Washington University in St. Louis, St. Louis, US

P096 HEPATO-PANCREATO-BILIARY SURGERY IN CANADA: WORKFORCE AND WAIT TIMES Janet Edwards, MD, MPH, Alexsander Bressan, MD, Sean C Grondin, MD, MPH, Indraneel Datta, MD, MScHEPM, Elijah Dixon, MD, MScEpi, Chad G Ball, MD, MScEpi, University of Calgary, Calgary, CA

P097 PANCREATIC TEXTURE-TAILORED RECONSTRUCTION TECHNIQUE IN PANCREATIC HEAD RESECTIONS: SUPERIORITY OF PANCREATOGASTROSTOMY (PG) VS. PANCREATICO-JEJUNOSTOMY (PJ) IN HIGH RISK ANASTOMOSES G Alsfasser, MD, J Bochow, MS, A L Kutsch, MS, E Klar, MD, B Rau, MD, University of Rostock, Rostock, DE

P098 PREDICTORS AND DIAGNOSTIC STRATEGIES OF EARLY STAGE PANCREATIC DUCTAL ADENOCARCINOMA: A RETROSPECTIVE REVIEW Hideyo Kimura, Takao Ohtsuka, Taketo Matsunaga, Yusuke Watanabe, Koji Tamura, Noboru Ideno, Teppei Aso, Yoshihiro Miyasaka, Junji Ueda, Shunichi Takahata, Kazuhiro Mizumoto, Masao Tanaka, Department of Surgery and Oncology, Graduate School of Medical Sciences Kyushu University, Fukuoka-city, JP

P099 CO-DELIVERY OF GEMCITABINE AND MI$-205 IN POLYMERIC MICELLES FOR THE TREATMENT OF PANCREATIC CARCINOMA Deepak Chitkara, PhD, Anupama Mittal, PhD, Stephen W Behrman, MD, Ram I Mahato, PhD, University of Nebraska Medical Center; University of Tennessee Health Science Center, Memphis, US

P100 DOES LAPAROSCOPIC DISTAL PANCREATECTOMY REDUCE THE RATE OF READMISSIONS? Janak A Parikh, MD, MSHS, Scott Bendix, MD, Farrukh Jabbar, MD, Michael J Jacobs, MD, FACS, St John Providence Hospital, Southfield, MI, Novi, US



POSTER LISTINGS

P101 EN BLOC TRANSECTION OF PANCREATIC PARENCHYMA AND SPLENIC VESSELS IN DISTAL PANCREATECTOMY: A SAFE AND NOVEL TECHNIQUE Janak A Parikh, MD, MSHS, Farrukh Jabbar, MD, Scott Bendix, MD, Michael J Jacobs, MD, FACS, St John Providence Hospital, Southfield, MI, Novi, US

P102 ISOLATED ROUX-EN-Y DRAINAGE OF THE PANCREATIC STUMP REDUCED THE AMYLASE LEVEL IN THE DRAINAGE FLUID AFTER DISTAL PANCREATECTOMY WITH EN-BLOC CELIAC AXIS RESECTION Ken-ichi Okada, Masaji Tani, Manabu Kawai, Seiko Hirono, Motoki Miyazawa, Atsushi Shimizu, Yuji Kitahata, Hiroki Yamaue, Second Department of Surgery, Wakayama Medical University, Wakayama, JP

P103 PANCREATIC ADENOCARCINOMA IN YOUNG PATIENTS: A SINGLE INSTITUTION EXPERIENCE OVER 32 YEARS Farzad Alemi, MD, Jessica Koller, MD, Sameer Damle, MD, Thomas Biehl, MD, Adnan Alseidi, MD, Scott Helton, MD, Flavio G Rocha, MD, Virginia Mason Medical Center, Seattle, US

P104 BENEFIT OF PANCREATICODUODENECTOMY WITH RESECTION OF PORTAL OR SUPERIOR MESENTERIC VEIN FOLLOWING CHEMORADIOTHERAPY IN PATIENTS WITH PANCREATIC DUCTAL ADENOCARCINOMA Shugo Mizuno, Masashi Kishiwada, Akihiro Tanemura, Yasuhiro Murata, Naohisa Kuriyama, Yoshinori Azumi, Masanobu Usui, Hiroyuki Sakurai, Masami Tabata, Shuji Isaji, Department of Hepatobiliary Pancreas and Transplant Surgery, Mie University, Tsu, Mie, JP

P105 PREDICTORS OF OUTCOME IN RESECTED AMPULLARY CARCINOMA, A SINGLE INSTITUTION EXPERIENCE Joyce Wong, MD, Zachary Thompson, PhD, Barbara Centeno, MD, Evita Henderson-Jackson, MD, Christy Chai, MD, Pamela J Hodul, MD, Moffitt Cancer Center, Harrisburg, US

P106 PANCREATICO-JEJUNOSTOMY ON ISOLATED LOOP AFTER PANCREATICODUODENECTOMY: THE INCIDENCE AND SEVERITY OF POSTOPERATIVE PANCREATIC FISTULA Gennaro Clemente, MD, AgostinoMaria De Rose, MD, Alessandro Coppola, MD, Gennaro Grande, MD, Lucia Ionta, MD, Marino Murazio, MD, Felice Giuliante, MD, Gennaro Nuzzo, MD, Department of Surgery-Hepatobiliary Unit; A. Gemelli Med School - Rome, Italy, Rome, IT

P107 POSTOPERATIVE NUTRITIONAL EVALUATION USING GERIATRIC NUTRITIONAL RISK INDEX (GNRI) FOR MATURE PATIENTS WITH PANCREATODUODENECTOMY Yuichi Kitagawa, MD, Yasuji Kawabata, MD, Ken Fujishiro, MD, Shinji Fukata, MD, Department of Surgery and Intensive Care, Division of Surgery National Center for Geriatrics and Gerontology, Obu, JP

P108 PROGNOSTIC IMPACT OF HUMAN EQUILIBRATIVE NUCLEOSIDE TRANSPORTER 1 AND RIBONUCLEOTIDE REDUCTASE SUBUNIT 1 EXPRESSION IN CHOLANGIOCARCINOMA PATIENTS TREATED WITH ADJUVANT GEMCITABINE-BASED CHEMOTHERAPY Hayato Sasaki, Yoshiaki Murakami, Kenichiro Uemura, Takeshi Sudo, Yasushi Hashimoto, Naru Kondo, Taijiro Sueda, Department of Surgery, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, JP

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Poster Listings

POSTER LISTINGS

P109 A NEW SURGICAL TECHNIQUE FOR PANCREATIC HEAD-BODY CANCER WITH SPLENIC ARTERY INVASION: PANCREATICODUODENECTOMY WITH THE SPLENIC ARTERY RESECTION (PD-SAR) Ryosuke Desaki, MD, Masashi Kisiwada, MDPhD, Syugo Mizuno, MDPhD, Akihiro Tanemura, MDPhD, Yasuhiro Murata, MDPhD, Yoshinori Azumi, MDPhD, Naohisa Kuriyama, MDPhD, Masanobu Usui, MDPhD, Hiroyuki Sakurai, MDPhD, Masami Tabata, MDPhD, Syuji Isaji, MDPhD, Department of Hepatobiliary Pancreas and Transplant Surgery, Mie University Graduate School of Medicine, Tsu, JPP110 SPYGLASS SINGLE OPERATOR PERORAL CHOLANGIOSCOPY (SOC) SEEMS PROMISING IN THE EVALUATION OF PRIMARY SCLEROSING CHOLANGITIS (PSC) RELATED BILIARY STRICTURES: A CASE SERIES AND INITIAL EXPERIENCE FROM A TERTIARY REFERRAL CENTER Antti Siiki, MD, Irina Rinta-Kiikka, MD, PhD, Tarmo Koivisto, MD, PhD, Kaija Vasama, MD, PhD, Juhani Sand, MD, PhD, Johanna Laukkarinen, MD, PhD, Dept. of Gastroenterology and Alimentary Tract Surgery1, Department of Clinical Radiology2, and Dept. of Pathology, Fimlab Laboratories3, Tampere University Hospital, Tampere, Finland, Tampere, FIP111 ROLE OF SURGICAL PALLIATION IN PATIENTS WITH PANCREATIC DUCTAL ADENOCARCINOMA (PDAC) Ammara Abbasi, MD, Ruby J Lo, MD, A. James Moser, MD, FACS, Jennifer F Tseng, MD, FACS, Charles M Vollmer Jr., MD, FACS, Mark P Callery, MD, FACS, Tara S Kent, MD, FACS, Department of Surgery, Beth Israel Deaconess Medical Center; Department of Surgery, University of Pennylvania, Boston, USP112 STAPLED GASTROJEJUNOSTOMY AND JEJUNOJEJUNOSTOMY ANASTOMOSIS REDUCES DELAYED GASTRIC EMPTYING AFTER PANCREATODUODENECTOMY WITH CHILD RECONSTRUCTION Yoshihiro Okuda, MD, Masashi Kishiwada, MD, PhD, Rie Sato, MD, PhD, Yasuhiro Murata, MD, PhD, Akihiro Tanemura, MD, PhD, Naohisa Kuriyama, MD, PhD, Yoshinori Azumi, MD, PhD, Shugo Mizuno, MD, PhD, Masanobu Usui, MD, PhD, Hiroyuki Sakurai, MD, PhD, Masami Tabata, MD, PhD, Shuji Isaji, MD, PhD, Hepatobiliary Pancreatic and Transplant Surgery, Mie University School of Medicine, Tsu, Japan, Tsu, JPP113 USEFULNESS OF GRADING OF PANCREATIC NEUROENDOCRINE TUMOR BY USING EUS-FNA SPECIMEN IN SELECTION OF OPERATIVE PROCEDURE BY COMBINATION WITH UICC-T FACTOR Kazuhisa Fujinaga, Masanobu Usui, MD, PhD, Akihiro Tanemura, MD, PhD, Naohisa Kuriyama, MD, PhD, Yoshinori Adumi, MD, PhD, Masashi Kishiwada, MD, PhD, Shugo Mizuno, MD, PhD, Hiroyuki Sakurai, MD, PhD, Masami Tabata, MD, PhD, Hiroyuki Inoue, MD, PhD, Hiroshi Imai, MD, PhD, Shuji Isaji, MD, PhD, Hepatobiliary Pancreatic and Transplant Surgery, Tsu, Mie, JPP114 PORTAL VEIN RESECTION IS ASSOCIATED WITH IMPROVED SURVIVAL AFTER PANCREATICODUODENECTOMY FOR PANCREATIC CANCER Prashant B Sukharamwala, MD, Krishen Patel, BS, Richard L Klein, Thomas W Wood, MD, Anthony F Teta, BS, Sharona B Ross, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, USP115 MULTIFOCAL PRE-INVASIVE PANCREATIC CANCER IN AN 18-YEAR-OLD-WOMAN Lindsey L Manos, PAC, Ashley Salamone, CRNP, Elliot K Fishman, MD, Anne Marie Lennon, MD, PhD, Ralph H Hruban, MD, Christopher L Wolfgang, MD, PhD, The Johns Hopkins Medical Institution, Baltimore, US



POSTER LISTINGS

P116 SMOKING HISTORY DOES NOT APPEAR TO PREDICT PATHOLOGY IN SURGICALLY RESECTED INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS Neda Rezaee, MD, Saami Khalifian, MS, John L Cameron, MD, Timothy M Pawlik, MD, MPH, PhD, Ralph H Hruban, MD, Elliot K Fishman, MD, Martin A Makary, MD, MPH, Anne Marie Lennon, MD, PhD, Christopher L Wolfgang, MD, PhD, FACS, Matthew J Weiss, MD, PhD, FACS, Department of Surgery, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland, Baltimore, US

P117 WITHDRAWP118 REGIONAL HOSPITAL CHARGES FOR PANCREATICODUODENECTOMY IN FLORIDA: LOCATION MATTERS Sharona B Ross, MD, Amanda E Smart, Carrie E Ryan, MS, Thomas W Wood, MD, Prashant B Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

P119 OUTCOMES FOLLOWING THE SELECTIVE APPLICATION OF LAPAROSCOPIC PANCREATICODUODENECTOMY Steven J Hughes, MD, Daniel Delitto, MD, Jose G Trevino, MD, Kevin E Behrns, MD, Department of Surgery, University of Florida, Gainesville, US

P120 WITHDRAWP121 THE ROLE OF PORTOMESENTERIC VEIN RESECTION AT TIME OF PANCREATODUODENECTOMY FOR PANCREATIC DUCTAL ADENOCARCINOMA Kengo Asai, MD, Victor Zaydfudim, MD, Sarah Perkins, Guido Sclabas, MD, Rory Smoot, MD, Mark Truty, MD, Kaye Reid Lombardo, MD, David Nagorney, MD, Michael Kendrick, MD, Karla Ballman, PhD, Michael Farnell, MD, Division of Gastroenterologic and General Surgery, Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, MN, USA, Rochester, US

P122 IRREVERSIBLE ELECTROPORATION CAN AUGMENT RESECTION IN LOCALLY ADVANCED PANCREATIC ADENOCARCINOMA John E Mullinax, MD, Vic Velanovich, MD, Robert C. G. Martin, MD, PhD, University of South Florida College of Medicine, University of Louisville College of Medicine, Tampa, US

P123 DIVISION OF THE PANCREAS DURING DISTAL PANCREATECTOMY: A RELIABLE AND SIMPLE TECHNIQUE WHICH RESULTS IN A VERY LOW FISTULA RATE John A Stauffer, MD, FACS, Horacio J Asbun, MD, FACS, Mayo Clinic Florida, Jacksonville, US

P124 PROGNOSTIC IMPACT OF PARA-AORTIC LYMPHNODES DISSECTION DURING PANCREATICODUODENECTOMY FOR CANCER Gennaro Nappo, MD, Domenico Borzomati, MD, PhD, FACS, Sergio Valeri, MD, Gianluca MascianA, MD, Paolo Luffarelli, MD, Giuseppe Perrone, MD, Roberto Coppola, MD, FACS, Campus Bio-Medico University of Rome, Rome, IT

P125 DOES LENGTH OF PREOPERATIVE ADMISSION IMPACT IN-HOSPITAL MORBIDITY AND MORTALITY AFTER PANCREATECTOMY? A POPULATION-BASED STUDY Clancy J Clark, MD, Shuja Ahmed, MD, Emeka Obiora, MD, Perry Shen, MD, Wake Forest Baptist Health, Winston Salem, US

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Poster Listings

POSTER LISTINGS

P126 WITHDRAWP127 SURVIVAL BENEFIT OF ADJUVANT THERAPY FOR RESECTABLE PANCREATIC CANCER PATIENTS TREATED WITH NEOADJVUANT THERAPY K J Duelge, BS, A N Krepline, BS, A Mahmoud, BS, B George, MD, P S Ritch, MD, B A Erickson, MD, K K Christians, MD, D B Evans, MD, S Tsai, MD, Medical College of Wisconsin, Milwaukee, US

P128 NEOADJUVANT THERAPY FOR PANCREATIC CANCER IN PATIENTS > AGE 75 J Miura, MD, A N Krepline, BS, K Duelge, BS, B George, MD, P S Ritch, MD, B A Erickson, MD, D B Evans, MD, K K Christians, MD, S Tsai, MD, Medical College of Wisconsin, Milwaukee, US

P129 CLINICAL CHARACTERISTICS OF NEWLY DIAGNOSED PANCREATIC ADENOCARCINOMA IN FAMILIAL PANCREATIC CANCER KINDREDS FROM A INSTITUTIONAL PANCREATIC CANCER REGISTRY Patricio M Polanco, MD, Murawid M Assifi, MD, Jordan M Knox, BA, Ruth E Dudley, MD, Amer H Zureikat, MD, David L Bartlett, MD, Herbert J Zeh, MD, Aatur Singhi, MD, Randall E Brand, MD, Melissa E Hogg, MD, Division of Surgical Oncology, Division of Gastroenterology, Department of Human Genetics, University of Pittsburgh Medical Center, Pittsburgh, US

P130 LONG-TERM FOLLOW-UP OF RESECTED SMALL (< 2 CM) ASYMPTOMATIC SPORADIC NON-FUNCTIONING PANCREATIC NEUROENDOCRINE TUMORS: CORRELATION BETWEEN TYPE OF RESECTION, HISTOPATHOLOGIC FEATURES, AND OUTCOME Giuseppe Malleo, MD, Anna Malpaga, MD, Paola Capelli, MD, Claudio Bassi, MD, Giovanni Butturini, PhD, Unit of Surgery B, The Pancreas Institute, University of Verona Hospital Trust; Unit of Pathology, The Pancreas Institute University of Verona Hospital Trust, Verona, IT

P131 LAPAROSCOPIC DISTAL PANCREATECTOMY WHAT IS THE DATA? Cherif N Boutros, MD, MSc, FACS, Lance Uradomo, MD, Mukul Khandelwal, MD, University of Maryland School of Medicine, University of Maryland Baltimore Washington Medical Center, Baltimore, US

P132 WITHDRAWP133 COST ANALYSIS OF OPEN AND LAPAROSCOPIC PANCREATICODUODENECTOMY: A SINGLE INSTITUTION COMPARISON John A Stauffer, MD, FACS, Marc Mesleh, MD, Horacio J Asbun, MD, FACS, Mayo Clinic Florida, Jacksonville, US

P134 MINIMALLY INVASIVE TREATMENTS OF PANCREATIC AND PERIAMPULAR CANCER: SIXTY SUCCESSFUL CASES Igor E Khatkov - 1,2, Professor, MD, PhD, Victor V Tsvirkun - 1, Professor, MD, PhD, Roman E Izrailov - 1,2, Professor, MD, PhD, Pavel S Tyutyunnik, MD, 1 - Moscow Scientific Research Institute of Gastroenterology; 2 - Moscow State University of Medicine and Dentistry, Moscow, RU

P136 OUTCOMES FOLLOWING DISTAL PANCREATECTOMY FOR CHRONIC PANCREATITIS: A SINGLE INSTITUTION EXPERIENCE OF 33 PATIENTS Nathan Avery, MD, Flavio Rocha, MD, Virginia Mason Medical Center, Seattle, US


TABLE OF CONTENTSOral Abstracts

ORAL ABSTRACTS

S001 DIAGNOSTIC LAPAROSCOPY TO DETECT OCCULT METASTATIC DISEASE PRIOR TO NEOADJUVANT CHEMORADIATION IN BORDERLINE RESECTABLE PANCREATIC DUCTAL ADENOCARCINOMA - A COST ANALYSIS June S Peng, Jeffrey Mino, Noaman Ali, Kevin M El-Hayek, Colin O’Rourke, Sricharan Chalikonda, R. Matthew Walsh, Cleveland Clinic Foundation, Cleveland, US

BACKGROUND: In patients with borderline resectable pancreatic ductal adenocarcinoma (PDAC), neoadjuvant chemoradiation offers a potential for curative resection. Current methods of radiographic staging can miss occult metastatic disease, which is reflected in the wide range of resectability rates after neoadjuvant therapy reported in the literature. This study aims to evaluate the outcomes of borderline resectable PDAC and assess the relative cost of utilizing staging diagnostic laparoscopy (SDL) as an adjunct to radiographic and endoscopic staging.

METHODS: This study is a retrospective review of patients presenting to a single tertiary care institution with borderline resectable PDAC since 2010. Patients underwent SDL at the discretion of their surgeon prior to starting neoadjuvant chemoradiation; SDL included biopsy of suspicious lesions, peritoneal washings, and placement of a central venous port for access. Eligible patients were identified from our institution’s electronic medical record and data on patient demographics, staging workup, and oncologic and surgical interventions were collected and analyzed. Patient level cost data, when available, was used to calculate total cost of care related to each patient’s pancreatic cancer treatment and a cost ratio was calculated to compare relative costs of SDL versus no SDL.

RESULTS: A total of 116 patients were identified for inclusion in the study. Five patients (4.3%) declined surgery, 2 patients (1.7%) were not offered surgery due to medical comorbidities, and 7 patients (6.0%) underwent attempted resection up front. The remaining 102 patients (88%) were candidates for neoadjuvant therapy and 76 (75%) underwent SDL. Nineteen of the 76 SDLs (25%) were positive with metastatic implants or positive cytology. Patients undergoing SDL were younger (63.6 vs 69.8 years, p=0.001); imaging characteristics of the primary tumor were comparable in the two groups, including mean size (3.0 vs 3.0cm, p=0.69) and encasement or involvement of an artery (13.4 vs 10.8%, p=0.77), vein (64.2 vs 64.9%, p>0.99), or both artery and vein (22.4 vs 24.3%, p>0.99). There were 81 patients who received neoadjuvant chemoradiation. In 55 patients with a previously negative SDL, 5 (9.1%) were unable to complete neoadjuvant therapy, 21 (38.2%) were found to have locally progressive or metastatic disease on restaging, 29 (52.7%) underwent attempted resection, and 20 (36.4%) were successfully resected. In 26 patients who underwent neoadjuvant chemoradiation without SDL, 7 (26.9%) were unable to complete neoadjuvant therapy, 11 (42.3%) progressed, 8 (30.8%) underwent attempted resection, and 6 (23.1%) were successfully resected. Relative cost of care, expressed as the ratio of the geometric mean costs in the SDL versus no SDL groups is 1.3 (0.9-1.9, 95% CI) for all patients in the study and 1.64 (1.1-2.6) for patients who ultimately underwent resection.

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CONCLUSION: The optimal management of patients with borderline resectable PDAC is debated. Experience at this institution demonstrates that 25% of patients with radiographically borderline resectable disease have occult metastasis detected by SDL at time of diagnosis, and these patients are spared aggressive therapy which is of little benefit. A cost comparison shows no statistically significant difference in overall costs for patients to undergo a SDL prior to neoadjuvant therapy.

S002 RISK OF VENOUS THROMBOEMBOLISM DURING NEOADJUVANT THERAPY FOR RESECTABLE AND BORDERLINE RESECTABLE (BLR) PANCREATIC ADENOCARCINOMA (PC) A N Krepline, B George, P S Ritch, B A Erickson, J P Thomas, A Mahmoud, E J Quebbeman, K Turaga, F M Johnston, T C Gamblin, K K Christians, D B Evans, S Tsai, Medical College of Wisconsin, Milwaukee, US

BACKGROUND: PC increases venous thromboembolism (VTE) risk. The impact of neoadjuvant therapy on VTE risk is unknown.

METHODS: From 2007-2013, neoadjuvant patients (pt) with resectable and BLR PC were identified. Radiographic reports from diagnosis to restaging, demographic, and clinicopathologic data were abstracted.

RESULTS: Seventy-nine resectable and 84 BLR PC pt undergoing neoadjuvant therapy were identified. From diagnosis to start of treatment, 10 pt (5 resectable and 5 BLR) were diagnosed with VTE - prevalence of 6.13%. VTE was associated with lower hemoglobin (11.97 vs. 13.17, p = 0.03) and AB blood type (20.0% vs. 2.73%, p = 0.05). Incident VTE developed in 17 pt (11.11%) - 4 (25.5%) resectable and 13 (76.40%) BLR. Three pt (17.65%) had pulmonary embolisms (PE) and 14 (82.35%)



ORAL ABSTRACTS

had deep venous thromboses (DVT). Ten pt developed VTE (58.82%) within the first 2 months of therapy. Thirteen (76.47%) were symptomatic (12 DVT and 1 PE). Of incident VTE, 6 (35.29%) were catheter related, 9 (52.94%) occurred remote from indwelling catheter, and 2 (11.76%) occurred in the absence of a catheter. Use of granulocyte colony stimulating factor (GCSF) was associated with VTE risk (41.18 vs. 16.91, p = 0.02). In a multivariate logistic regression, receipt of GCSF (odds ratio 3.46, p = 0.07) and BLR clinical stage (odds ratio 3.08, p =0.07) were associated incident VTE.

CONCLUSIONS: PC patients undergoing neoadjuvant therapy are at significant risk of VTE. Advanced clinical stage and the use of GCSF may be associated with greater VTE risk. Prophylactic anticoagulation may be indicated in high-risk patients.

S003 IMPACT OF SURGICAL RESECTION AFTER CHEMORADIOTHERAPY FOR LOCALLY ADVANCED UNRESECTABLE PANCREATIC DUCTAL ADENOCARCINOMA Masashi Kishiwada, PhD, MD, Rie Sato, MD, Yasuhiro Murata, PhD, MD, Akihiro Tanemura, PhD, MD, Naohisa Kuriyama, PhD, MD, Yoshinori Azumi, PhD, MD, Shugo Mizuno, PhD, MD, Masanobu Usui, PhD, MD, Hiroyuki Sakurai, PhD, MD, Masami Tabata, PhD, MD, Shuji Isaji, PhD, MD, Hepatobiliary Pancreatic and Transplant Surgery, Mie University School of Medicine, Tsu, JP

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) with involvement of the superior mesenteric artery and/or celiac axis was commonly considered unresectable. For selected patients with locally advanced PDAC, chemoradiotherapy may offer the potential for margin-negative (R0) resection, resulting in improvement of prognosis. At our institution, we have been performing chemoradiotherapy followed by surgery (CRT-S) for PDAC. The aim of this study was to evaluate the efficacy of CRT-S for PDAC, particularly in the locally unresectable (UR) cancer defined by NCCN pancreatic cancer guidelines (2013). These include >180 degree encasement of the superior mesenteric artery (SMA), unreconstructive portal vein occlusion, aortic invasion, or celiac encasement.

METHODS: From February 2005 to October 2013, 191 consecutive patients with cytologically/histologically proven PDAC (UICC-T3 87 cases,-T4 104 cases) had been enrolled for our CRT-S protocol. CRT regimen: radiation therapy (total dose of 45 to 50.4 Gy, 25 to 28 fractions) with chemotherapy which included gemcitabine (800mg/m2, day1,8,22,29, 2005.2-2011.10, n=124) or gemcitabine (600mg/m2,day8,22,36,50)+ oral S-1, active combination of tegafur, gimeracil and oteracil (60/m2, day1-21 and day 29-49, 2011.11-2013.10, n=67). These patients were retrospectively classified into three respectability groups based on four-phase dynamic CT. The patients underwent curative-intent resection after reassessment by response of CRT completion. At the time of reassessment, we determined that curative-intent resection was possible when the following findings on MDCT were observed: no stenosis or change of shape in the celiac axis and SMA and the absence of metastatic lesions in other distant organs. The primary endpoint was overall survival, secondary one was R0 resection.

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RESULTS: The 191 patients were reclassified as resectable in 17 patients, borderline resectable in 92 and UR in 82. Among UR patients, completion rate of CRT was 95.1% (78/82). The 19 patients (23.1%) were precluded from surgery due to distant metastasis at the time of restaging. The 35 patients (42.7%) underwent surgical resection: the time from initial treatment to resection (median) was 3.2 months (range:2 to 12). The rate of R0 resection was 57.1% (20/35). The 2-year survival rate and median survival time (MST) were 24.8% and 13.3 months in the entire 82 patients, being significantly better in 35 patients with resection than in 47 patients without resection (38.2% vs. 20.1%, 23.8 vs.10.3 months, P=0.0088). Interestingly, in the resected cases, there was no significant difference in survival between R0 (n=20) and R1(n=13) (43.7% vs. 31.8%, 23.8 vs. 12.1 months, P=0.262).

CONCLUSION: CRT-S can select the patients with locally advanced unresectable PDAC who are likely to benefit from aggressive resection.

S004 A COMPREHENSIVE ASSESSMENT OF NEOADJUVANT THERAPY FOR PANCREATIC ADENOCARCINOMA: RESULTS FROM THE NATIONAL CANCER DATABASE (NCDB) Russell S Lewis, BS, Jeffrey A Drebin, MD, PhD, Douglas L Fraker, MD, Charles M Vollmer, MD, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, US

INTRODUCTION: Limited, early experience from specialty centers suggests neoadjuvant therapy for pancreatic adenocarcinoma (PDAC) holds promise for enhancing patient selection, improving survival, or both. A comprehensive, contemporary assessment of its utilization on a national scale is lacking.

METHODS: Surgical patients with diagnoses of invasive PDAC between 1998-2010 were identified from the NCDB. Neoadjuvant patients (NA) were defined as those who received chemotherapy and/or radiation before surgery. NA and surgery-first patients (SF) were compared and survival analysis was conducted on patients treated between1998-2005.

RESULTS: Among 232,539 PDAC patients overall, 43,724 were SF. 2,680 NA cases (5% of surgeries) were contributed by 532 institutions, 10 of which provided 31% of the cases. The use of NA doubled (6-12% of surgical PDAC) between 2006-2010. One-third of NA patients had chemotherapy only. When compared to SF patients, NA patients were treated in academic centers more often (66.4% vs. 51.9%; P<0.001). Charlson comorbidity scores did not differ. Only 17% of NA patients were clinical T4, suggesting few were locally advanced. Median days from diagnosis to surgery were 122 in NA patients. Mean postoperative stay was shorter in NA patients (11.0d vs. 12.0d; P<0.001). 30-day surgical mortality for NA was 2.8% vs. 4.9% for SF (P<0.001). Additional systemic therapy was applied to 29.3% of NA patients postoperatively. NA patients had median survival from diagnosis of 19.9 vs. 15.3m in SF (P<0.001); however, long-term survival was equivalent (5-year=14% in both). Survival benefit was observed for NA in all Stages except Stage I. There was significant regional and institutional variation in NA survival rates.

CONCLUSION: National utilization of NA therapy has increased significantly in recent years, and now represents a common treatment path for patients with



ORAL ABSTRACTS

PDAC. Although this does not reflect an intention-to-treat analysis, NA functions well as a patient selection technique, as it improves postoperative outcomes. Furthermore, NA therapy appears to improve survival in advanced stage disease but not in earlier tumors.

S005 DOES THE USE OF NEOADJUVANT THERAPY FOR PANCREATIC ADENOCARCINOMA INCREASE POSTOPERATIVE MORBIDITY AND MORTALITY RATES? Amanda B Cooper, MD, Abhishek Parmar, MD, Taylor S Riall, MD, PhD, Bruce L Hall, MD, PhD, MBA, Matthew H Katz, MD, Thomas A Aloia, MD, Jason B Fleming, MD, Henry A Pitt, MD, MD Anderson Cancer Center, University of Texas Medical Branch at Galveston, Washington University at St. Louis, Temple University School of Medicine, Houston, US

INTRODUCTION: The effects of neoadjuvant therapy on postoperative complications following pancreatectomy for pancreatic cancer have not been well studied. Using prospectively collected data from the NSQIP Pancreatectomy Demonstration Project, we compared postoperative outcomes for patients with pancreatic adenocarcinoma treated with a surgery-first vs. neoadjuvant therapy-first approach.

METHODS: We included all patients with pancreatic adenocarcinoma captured within the NSQIP Pancreatectomy Demonstration Project from November 2011 to December 2012. Patients were classified according to neoadjuvant therapy status (chemotherapy and/or radiation). Patients receiving neoadjuvant therapy were then further classified as having received chemotherapy alone or radiation with or without chemotherapy. The groups were compared using the Fisher’s exact test with significance set at p<0.05.

RESULTS: Of the 1,567 patients with pancreatic cancer identified, 199 patients received neoadjuvant therapy—99 patients (6.3%) received neoadjuvant chemotherapy alone and 100 (6.4%) received neoadjuvant (chemo)radiation. Demographic data were not notably different between the surgery-first and the neoadjuvant therapy groups. Patients treated with neoadjuvant therapy were more likely to need a vascular resection than patients treated with surgery first (41.5% vs. 17.3%, p<0.0001). Patients treated with any neoadjuvant therapy were also more like to undergo biliary stenting (58.9% vs. 44.5%, p=0.0006) and were less likely to have a laparoscopic resection (6.0% vs. 8.6%, p=0.05) than patients treated with surgery first. Patients in the neoadjuvant group had a mean operative time of 6.9 hours compared to 5.9 hours for patients in the surgery-first group (p<0.0001); however, their mean length of stay (10.4 days) was not longer than that of the surgery-first group (11.1 days, p=0.32). The 30-day mortality rate did not differ for patients in the neoadjuvant therapy compared to the surgery-first groups (2.0% vs. 1.5%, p=0.56). Overall postoperative morbidity also did not differ between the two groups (56.3% vs. 52.9%, p=0.34). Postoperative mortality and the incidence of most 30-day complications did not differ significantly based on use of neoadjuvant therapy; however, patients treated with neoadjuvant therapy were significantly less likely to have a deep organ space infection (3.0%

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vs. 11.5%, p=0.0004) and patients treated with neoadjuvant radiation were less like to develop a pancreatic fistula (7.3% vs. 15.5%, p=0.03).

CONCLUSIONS: Only 12.7% of patients with pancreatic adenocarcinoma captured in the Pancreatectomy Demonstration Project were treated with neoadjuvant therapy. Our data suggest that patients receiving neoadjuvant therapy in this dataset had more extensive disease (more frequently requiring vascular resection with a longer mean operative time). Despite this, neoadjuvant therapy was associated with lower rates of deep organ-space infections and neoadjuvant radiation was associated with lower rates of pancreatic fistula. Concern over increasing rates of postoperative complications should not deter the use of neoadjuvant therapy for pancreatic cancer.

S006 NEOADJUVANT CHEMORADIATION VERSUS NEOADJUVANT CHEMOTHERAPY PRIOR TO PANCREATICODUODENECTOMY FOR PANCREATIC CANCER Pragatheeshwar Thirunavukarasu, MD, Kristopher Attwood, Boris W Kuvshinoff, MD, Steven J Nurkin, MD, Department of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, US

BACKGROUND: Neoadjuvant therapy has been increasingly utilized for both borderline and even earlier stage resectable pancreatic adenocarcinoma prior to pancreaticoduodenectomy. Little is known regarding the relative benefit of combination chemoradiation compared to chemotherapy alone in the neoadjuvant setting. We sought to compare survival of patients who underwent neoadjuvant chemoradiation (NeoCR) with those who underwent chemotherapy alone (NeoC) prior to surgical resection.

METHODS: We extracted data on all patients who underwent pancreaticoduodenectomy for pancreatic adenocarcinoma between 1998 and 2006 from the National Cancer Data Base (NCDB). Demographic, co-morbid status and clinicopathologic variables were collected and reviewed. Patients that received NeoC were compared to those that received NeoCR. Patients were excluded if they had T4 or M1 disease on final pathology. Survival analysis was performed using the Log-rank test.

RESULTS: We identified 285 patients that had neoadjuvant therapies prior to a pancreaticoduodenectomy. 201 patients had NeoCR and 85 had NeoC only. There were no statistically significant differences (P>.05) in the mean age, sex distribution, co-morbid conditions or T-stage between both groups. NeoCR was associated with a significantly higher rate of node-negative (N0) disease on pathological staging compared to NeoC (67.5% vs. 48.1%, P=.004) and a statistically non-significant trend towards lower margin positivity (13.1% vs. 22.8%, P=.07). There was no difference in the 30-day readmission rate after surgery (9.6% NeoCR vs. 6.2% NeoC, P=.50). The median survival with NeoC (24.4 months, 95% CI 28.2 – 41.5 months) and NeoCR (21.4 months, 95% CI, 18.0-24.82 months) were not different (P=.40) (Figure 1). Subset analysis of pathologically N0 patients showed marginal, although non-significant, survival benefit to NeoC over NeoCR (median survival, 95% CI; 38.1 months, 27.4-44.7 vs. 23.9 months, 19.1-27.0, P=.12)



ORAL ABSTRACTS

CONCLUSION: Chemoradiation in the neoadjuvant setting of pancreaticoduodenectomy for pancreatic cancer was associated with a higher rate of pathologically node-negative disease and a marginally lower positive margin rate than chemotherapy alone. Chemoradation did not improve overall survival. On the contrary, there was a non-significant trend towards decreased early survival associated with the use of radiation, especially in N0 disease. Prospective studies are needed in the future given the lack of pre-operative staging information and potential selection bias associated with the current study.

S007 CHANGES IN BODY COMPOSITION DURING PREOPERATIVE THERAPY FOR RESECTABLE PANCREATIC CANCER: DO THEY MATTER? Amanda B Cooper, MD, David Fogelman, MD, Holly M Holmes, MD, Rebecca S Slack, MS, Aparna Balachandran, MD, Naveen Garg, MD, Maria Q Petzel, Douglas B Evans, MD, Gauri R Varadhachary, MD, Robert A Wolff, MD, Christopher Crane, MD, Jeffrey E Lee, MD, Jason B Fleming, MD, Matthew H Katz, MD, MD Anderson Cancer Center, Medical College of Wisconsin, Houston, US

BACKGROUND: Sarcopenia (loss of muscle mass) predicts perioperative complications and delayed recovery after cancer surgery, and poor survival following de novo pancreatectomy in patients with pancreatic adenocarcinoma. However, the impact of sarcopenia on outcomes of pancreatic cancer patients treated with neoadjuvant therapy is unknown. We sought to characterize changes in body composition of pancreatic cancer patients treated with preoperative

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chemoradiation to determine the prevalence of baseline and treatment-associated sarcopenia and any association with survival.

METHODS: We examined the pretreatment and preoperative CT scans of all 90 patients with potentially resectable pancreatic cancer enrolled on a previously-reported phase II trial of neoadjuvant chemotherapy and chemoradiation. We computed normalized cross-sectional areas (CSA) of skeletal muscle (SKM), visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) at the L3 vertebral level. Sarcopenia was defined using gender-specific norms and evaluated in the context of prospectively-acquired clinical data.

RESULTS: At trial enrollment, 46 (52%) patients were sarcopenic, 53 (59%) were overweight or obese, and 21 (24%) were both. After neoadjuvant therapy (median 4.2 months), CSA (cm2/m2) decreased for each compartment [SKM 47.6 vs 46.3 (p=0.004), VAT 45.1 vs 41.2 (p=0.01), and SAT 53.0 vs 15.9 (p<0.001)] and 9 (23%) patients without baseline sarcopenia developed sarcopenia. Among all enrolled patients, neither pre- nor post-treatment sarcopenia were associated with successful pancreatectomy, progression-free, or overall survival (all p >0.05). However, among patients who underwent resection, patients who had large decreases in SKM prior to pancreatectomy had a shorter median disease-free survival than patients who had smaller decreases or increases in SKM during therapy (p=0.05).

CONCLUSIONS: In this first report of the changes in body composition that may occur in association with preoperative therapy, we demonstrated that sarcopenia is prevalent in patients with resectable pancreatic cancer upon diagnosis, and that preoperative therapy is associated with a further decline in SKM. Although our data suggest that baseline or treatment-associated sarcopenia alone may not portend a poor prognosis when neoadjuvant chemoradiation is employed, an absolute decrease in SKM may be associated with shorter disease-free survival among those patients who undergo resection after neoadjuvant therapy. Further studies are necessary to determine which alterations in body composition impact oncologic outcomes in patients treated with preoperative therapy, and how such alterations can be modulated to optimize treatment outcomes.

S008 PROSPECTIVE RANDOMIZED CONTROLLED STUDY COMPARING OUTCOME BETWEEN STANDARD RESECTION AND AN EXTENDED RESECTION THAT INCLUDED DISSECTION OF THE NERVE PLEXUS AND VARIOUS LYMPH NODES IN PATIENTS WITH PANCREATIC HEAD CANCER Jin-Young Jang, Mee Joo Kang, Jin Seok Heo, Seong Ho Choi, Dong Wook Choi, Sang Jae Park, Dong Sup Yoon, Hee Chul Yu, Koo Jung Kang, Sang Geol Kim, Sun-Whe Kim, Department of Surgery, Seoul National University & Korean Pancreatic Surgery Club, Seoul, KR

INTRODUCTION: Despite several previous RCTs on the extent of surgery in pancreatic cancer, many surgeons have tried to perform more extended resection due to several pitfalls of those studies. The aim of this study is to prospectively evaluate survival benefit of dissection of the nerve plexus and lymphadenectomy in the patients with the pancreatic head cancer.



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METHODS: A total of 244 patients was enrolled; of these, 200 were randomized to undergo standard (SR) or extended resection (ER), with the latter including the dissection of additional lymph nodes and the right half of the nerve plexus around the superior mesenteric artery and celiac axis. We analyzed 167 patients from 7 centers who fulfilled all of the required criteria.

RESULT: Operation time was longer and estimated blood loss was higher in the ER than in the SR group, but the R0 resection rate was comparable. Mean number of lymph nodes retrieved per patient was higher in the ER than in the SR group (33.7 vs. 17.3, p<0.001). The morbidity rate was slightly higher in the ER than in the SR group. There were 2 in-hospital deaths only in the ER group. Median survival after R0 resection was similar in the ER and SR groups 18.0 vs. 19.0 months, p=0.239) regardless of lymph node metastasis. Adjuvant chemoradiation had a positive impact on overall survival.

CONCLUSION: This study suggests that extended lymphadenectomy with nerve plexus dissection does not have a significant survival benefit compared with SR in pancreatic head cancer. The authors note that this standard resection can be done safely and efficiently, and does not in any way sacrifice oncologic efficacy or long-term survivorship when compared to patients undergoing an extended pancreaticoduodenal resection.

S009 MICROSCOPIC RESIDUAL TUMOR AFTER PANCREATICODUODENECTOMY FOR CANCER. PRELIMINARY RESULTS OF A MULTICENTRIC PROSPECTIVE RANDOMIZED TRIAL Roberto Coppola, MD, FACS, Domenico Borzomati, MD, Phd, FACS, Sergio Valeri, MD, Gennaro Nappo, MD, Michela Amato, MD, Giuseppe Perrone, MD, Andrea Onetti Muda, MD, Campus Bio-Medico University of Rome, Rome, IT

INTRODUCTION/BACKGROUND: Resection margin and lymph-node status after Pancreatico-Duodenectomy (PD) for cancer are the most powerful prognostic factors. Recent studies showed that a standardized pathological evaluation of the specimen increases the rate of microscopic residual tumour (R1) and nodal metastases after PD for cancer. We report the preliminary results of a multicentric prospective randomized study that compared standardized Vs non-standardized methods to evaluate the surgical specimen.

MATERIAL AND METHODS: Surgical specimens after PD performed for ampullary, biliary and pancreatic carcinoma were eligible for inclusion. Four different pancreatic surgery Units took part into the study:

Campus Bio-Medico University of Rome; Humanitas Institute of Milan (Surgeons: M. Montorsi, A. Zerbi. Pathologist: P. Spaggiari); University of Pisa (Surgeons: U. Boggi, F. Vistoli. Pathologist: D. Campani); University of Katowice (Surgeon: S. Mrowiec. Pathologist: L. Liszka)

Eligible cases were randomly allocated to receive two different methods of pathological evaluation:

1) GROUP A: the specimen was evaluated with the standardized method (Verbeke CS et Al. in Br. J. Surg. 2006; 93; 1232–1237).

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2) GROUP B: the specimen was evaluated with the method conventionally used by each centre.

The primary endpoint of the study was to verify if the standardized method determines a significant variation of R1 rate. The secondary endpoints were the evaluation of “T” and “N” status, number of examined blocks and number of examined lymph-nodes in the two groups.

RESULTS: From March 2013 until now, we randomly allocated 29 and 27 specimens to be managed with the standardized and the conventional method respectively. At final histology:

• 13 cases (23.2%) resulted ampullary cancer (group A: 9 patients, group B: 4 patients, p = n.s.)

• 8 cases (14.3%) resulted distal common bile duct cancer (group A: 5 patients, group B: 3 patients, p = n.s.)

• 35 cases (62.5%) resulted pancreatic head ductal adenocarcinoma (group A: 15 patients, group B: 20 patients, p = n.s.)

Mean size of the tumor was 2.59 cm (group A: 2.43 cm, group B: 2.77 cm, p = n.s.). R1 resection rates were 58.6% (group A) and 40.7% (group B) (p < 0.05). Average number of examined blocks was 44,4 (group A) and 23,4 (group B) (p < 0.05). Mean number of examined lymphnodes was 34,8 (group A) and 21,9 (group B) (p < 0.05). Metastatic lymphnodes were found in 72.4% (group A) and in 63.0% (group B) (p < 0.05).

DISCUSSION: This is the first prospective randomized study focusing the role of pathological evaluation of the specimen after PD for cancer. Preliminary results of our study confirm that the use of the standardized method increases the incidence of R1 resections, the number of examined lymph-nodes and the rate of nodal metastases. If definitive results of the present study will confirm these preliminary data, we should assume that at least two third of PD for cancer can not be considered “radical resections”.

S010 MINIMALLY INVASIVE PANCREATODUODENECTOMY: IS THE LEARNING CURVE SURMOUNTABLE? Attila Nakeeb, MD, Abishek Parmar, MD, Taylor S Riall, MD, PhD, E Molly Kilbane, RN, Bruce L Hall, MD, PhD, MBA, Henry A Pitt, MD, Indiana University School of Medicine, University Texas Medical Branch Galveston, Indiana University Health, Washington University School of Medicine, Temple University School of Medicine, Philadelphia, US

BACKGROUND: Minimally invasive pancreatoduodenectomy (MIPD) has been introduced in recent years at a few specialized centers. Both laparoscopic and robotic Whipple procedures have been mastered by a small number of surgeons around the world. Even in these expert hands, the learning curve has been steep, but patient safety issues have not been reported. However, the generalizability of this procedure has yet to be established. Therefore, the aim of this analysis was to determine whether the outcomes of MIPD are comparable to open surgery in a contemporary, multicenter cohort.



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METHODS: From November 2011 through December 2012, 1,781 patients underwent pancreatoduodenectomy (PD) at 43 institutions participating in the American College of Surgeons – National Surgical Quality Improvement Program (ACS-NSQIP) Pancreatectomy Demonstration Project. MIPD included laparoscopic, hand-assisted, robotic and robotic-assisted cases. MIPD was initiated in 131 patients (7.4%) at 21 centers. The mean and median cases per institution were six and three, respectively, and 66 (50%) were converted to open surgery. MIPD was completed at 13 institutions with the mean and median number of cases per institution being five and two, respectively. Major morbidity was defined as ACS-NSQIP serious morbidity plus clinically significant pancreatic fistulas. Outcomes for MIPD (completed plus converted) were compared to open PD by standard statistical analyses.

RESULTS: Minimally invasive (completed plus converted) and open patients were similar with respect to age, gender, race, ASA class, BMI, cardiopulmonary disease, diabetes, smoking, vascular resection and drain management. Minimally invasive converted patients had higher BMI’s (p<0.02) and were more likely to undergo vascular resection (p<0.01). Outcomes for Open and MIPD (completed plus converted) were:

Procedure Operative Time

Septic Shock Reoperation Major Morbidity

30-day Mortality

Open PD 6.1 hr 3.7% 3.5% 44.4% 1.8%MIPD 7.5 hr* 11.5%* 11.0%* 55.0%† 4.7%†

*p<0.01, † p <0.04 vs Open PD

CONCLUSIONS: This analysis suggests that compared to open surgery minimally invasive pancreatoduodenectomy (MIPD) takes longer and is associated with significantly increased major morbidity and mortality. In 2012, MIPD was attempted at many specialized centers, but half of the cases were converted to open surgery. For MIPD to become generalizable, improved developmental paradigms will be required.

S011 TOTAL LAPAROSCOPIC PANCREATICODUODENECTOMY FOR PANCREATIC DUCTAL ADENOCARCINOMA: ONCOLOGIC ADVANTAGES OVER OPEN APPROACHES? Kristopher P Croome, MD, MS, Michael Farnell, MD, Mark J Truty, MD, Kaye Reid-Lombardo, MD, Florencia G Que, MD, David M Nagorney, MD, Michael L Kendrick, MD, Mayo Clinic, Rochester, US

OBJECTIVE(S): Advantages of total laparoscopic pancreaticoduodenectomy(TLPD) include less blood loss and shorter hospital stay compared to open pancreaticoduodenectomy(OPD). Published oncologic outcomes of TLPD are limited by sample size and grouping of various cancer types. Our aim was to evaluate the oncologic outcomes of TLPD and OPD in patients with pancreatic ductal adenocarcinoma(PDAC).

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METHODS: Single institution, retrospective review of all patients undergoing TLPD(n=108) and OPD(n=214) for PDAC from July 2007 to July 2013.

RESULTS: Neoadjuvant therapy, tumor size, node positivity and margin positive resection were not different between the two groups. Median hospital stay was greater in the OPD group (9 vs 6 days, p<0.001). A greater proportion of patients in the OPD group had a delay of greater than 8weeks from surgery to adjuvant chemotherapy, 41% and 27% respectively (p=0.01). The proportion of patients with a delay of more than 90days or did not receive adjuvant treatment was also greater in the OPD(12%) compared to the TLPD(5%) group(p=0.04). Median follow-up was 1.5years. Overall survival was not different between the two groups (p=0.22), however, progression free survival was greater in the TLPD group(p=0.03).

CONCLUSIONS: TLPD not only provides the typical benefits of MIS approaches, but in patients with PDAC it may also prevent delayed initiation or cancellation of adjuvant therapy. In comparable patients, this study also demonstrated improved progression free survival for patients undergoing TLPD.

S012 PRELIMINARY RESULTS OF A SWEDISH, MR BASED, SCREENING PROGRAM FOR INDIVIDUALS AT RISK FOR PANCREAS CANCER Marco Del Chiaro, MD, PhD, Caroline Verbeke, MD, PhD, Nils Albiin, MD, PhD, Associate, Professor, Nikolaos Kartalis, MD, PhD, Stephan L Haas, MD, PhD, Ralf Segersvard, MD, PhD, Ake Andren-Sandberg, MD, PhD, Professor, Matthias Lohr, MD, PhD, Professor, Division of Surgery, Department of Clinical Science, Intervention and Technology (CLINTEC). Karolinska Institutet - Stockholm, Sweden, Stockholm, SE

INTRODUCTION: Ten % of all pancreatic cancers can be hereditary. A screening program for the individuals at risk (IAR) is recommended, but no defined surveillance modalities are available.

AIM: To analyze the frequency of findings in IAR

METHODS: From 2010 to 2013, all the patients with a “genetic risk” to develop pancreas cancer and referred to the Karolinska University Hospital, were included in a MR based surveillance program. All patients were investigated for the most common genetic mutation associated with pancreas cancer.

RESULTS: Forty patients were enrolled. There were 24 female and 16 man. The mean age was 49.9. The mean length of follow-up was 12.9 (± xx) months. The number of relatives affected by pancreas cancer was 5 in 2 patients (5%), 4 in 5 (12.5%), 3 in 17 (42.5%), 2 in 14 (35%) and 1 in 2 (5%). In 4 patients (10%) a p16 mutation was found, in 3 a BRCA 2 mutation (7.5%), in 1 a BRCA 1 mutation (2.5%). In 16 patients (40%) a suspect lesion was found in the pancreas with MR. Fourteen (35%) had an IPMN and 2 (5%) a pancreas cancer. Five patients (12.5%) required surgery and the remaining 37 continue with the surveillance program.

CONCLUSIONS: During a median follow-up of just about a year, we detected pancreatic lesions in about 40% of our patients, of which five underwent surgery. Despite the relatively short time, the surveillance program in IAR seems to be effective.



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S013 EARLY DETECTION OF PANCREATIC INTRAEPITHELIAL NEOPLASIA USING NON-INVASIVE IMAGING TO LOCALIZE AND GRADE PROTEASE ACTIVITY Dana A Dominguez, BS, Michael Paige, PhD, Fiore Cattaruzza, PhD, Anthony J O’Donoghue, PhD, Nilotpal Roy, PhD, Elliot S Seeley, MD, PhD, Matthias Hebrok, PhD, Kimberly S Kirkwood, MD, Charles S Craik, PhD, University of California, San Francisco, San Francisco, US

Patients with hereditary or chronic pancreatitis or IPMN are at increased risk of pancreatic cancer and undergo surveillance imaging with the hope of early detection, yet differentiation between benign, atypical or dysplastic lesions, and invasive cancers is inaccurate. Recently, the Sauer lab showed that cathepsin B and L activities correlate with PanIN severity and PDAC. Non-invasive functional imaging of proteolytic activity offers a promising strategy to grade the severity of dysplasia in the pancreas. We determined if proteolysis could be labeled in live animals and whether the activity relates to severity of dysplasia. We developed a novel in-vivo probe that deposits near-infrared fluorophores or radioisotopes at sites of proteolysis for non-invasive detection in live animals. Real-time measurement is enabled through a non-interfering localization mechanism that deposits probe on cellular membranes adjacent to the site of proteolytic activity and is amplified by the presence of phosphatidylserine.

Our technology, called Restricted Interaction Peptides (RIPs) serves to take advantage of this unregulated proteolysis. RIP probes are modified forms of spontaneous membrane binding peptides with addition of a cleavable targeting module and an imaging agent (Fig 1). For this study, we used a Cy5.5 tag, that was visualized using near infrared spectrometry at a dose of 5 nmol with no obvious harmful effects. For this proof of principle study, we compared probe deposition in the following mice: LSL-Kras(G12D/+);Pdx-1-Cre PDAC, wild type C57BL/6, cerulein-injected acute pancreatitis, and TNBS induced chronic pancreatitis and a novel model of IPMN that develops sequential PanINs and invasive cancer (LSL-KRAS(G12D/+) brg1 -/-).

As expected, there was a 5-fold increase in PANC-RIP probe deposition in acute pancreatitis as compared with both chronic pancreatitis and no probe controls. This activation was confirmed to be highly localized to the pancreas through ex-vivo examination of organs in isolation including liver, heart and lung. PDAC mice had significanty increased signal in both in-vivo imaging, as well as ex-vivo imaging of the respective pancreata as compared with both healthy controls and TNBS-chronic pancreatitis mice (Fig. 2). Ex-vivo immunofluorescence imaging of cryosections from animals with PDAC showed site-specific accumulation on epithelial cells, not on leukocytes or in stroma. A dose-response was seen with less probe accumulation in PanINs 1 and 2 and more in PanIN-3, with brightest signal in areas of invasion. All areas of PanIN-3 or invasive cancer showed increased probe signal. Similarly, in the IPMN mouse, probe was identified in PanINs and the highest activity was seen in cysts that had degenerated to PDAC (Fig. 3).

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Our preliminary data suggests that proteolytic activity increases during carcinogenesis and may be a useful tool for grading cellular atypia in the pancreas. Our novel RIP probe may provide a useful tool for non-invasive functional imaging using nanomolar doses, that offers the potential to detect PanIN-3s in patients with chronic pancreatitis and to discriminate benign from malignant cystic lesions in IPMN.

Fig. 1:

Fig. 2: Fig. 3:



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S014 ROLE OF CYB5A IN PANCREATIC CANCER: CORRELATION WITH CLINICAL OUTCOME AND FUNCTIONAL CHARACTERIZATION IN THE MODULATION OF AUTOPHAGY AND ONCOGENIC PHENOTYPES Elisa Giovannetti1, MD, PhD, Niccola Funel2,5, PhD, Amir Avan1, PhD, Qiuyan Wang3, PhD, Tonny Lagerweij4, PhD, Luca E Pollina, MD, Fabio Caniglia5, MD, Vittorio Perrone5, MD, Godefridus J Peters1, PhD, Thomas Wurdinger4, Md, PhD, Giuseppe Giaccone3, MD, PhD, Ugo Boggi5, MD, Departments of 1Medical Oncology, and 4Neurosurgery & Pediatric Oncology/Hematology, VU University Medical Center; 2Division of General and Transplant Surgery and 5Division of Surgical Pathology, University of Pisa, Pisa, 3Medical Oncology Branch, Nati, Pisa, IT

INTRODUCTION: Pancreatic ductal adenocarcinoma (PDAC) carries one of the worst prognoses of any major malignancy and exhibits profound chemoresistance. The inefficacy of currently available therapeutic strategies has been attributed to the dense desmoplastic reaction, which reduces drug penetration, and to the high rate of genetic alterations affecting multiple pathways. We previously investigated genomic imbalances using array comparative genomic hybridization in a cohort of 44 radically resected patients, the largest PDAC series ever investigated by array-comparative genomic hybridization. In this series, the median overall survivals (OS) for patients with and without loss of the cytoband 18q22.3 were 7.6 and 21.4 months, respectively. In agreement with previous findings, CPGL reduced proliferation and inhibited migration in SU.86.86 cells carrying FLAG-tagged CPGL. However, knockdown of CPGL in the PANC-1 cells did not affect proliferation, cell cycle distribution, and wound healing. The aim of this study was to evaluate whether the mRNAs and/or proteins coded by the genes in the 18q22.3 cytoband were associated with outcome in two cohorts of radically resected patients and one cohort of metastatic PDAC patients.

MATERIALS AND METHODS: We studied mRNA/protein expression in radically resected (n = 130) and metastatic patients (n = 50). The role of CYB5A was tested in 11 PDAC cell lines and five primary cultures through retrovirus-mediated upregulation and small interfering RNA using wound-healing, invasion, annexin-V, electron microscopy, and autophagic assays, as well as autophagy genes and kinases arrays. CYB5A+ orthotopic models (n = 6 mice/group) were monitored by Firefly and Gaussia-luciferase bioluminescence, magnetic resonance imaging, and high-frequency ultrasound. Data were analyzed by t test, Fisher exact-test, log-rank test and Cox proportional hazards models. All statistical tests were two-sided.

RESULTS: Both resected and metastatic patients with low mRNA or protein expression of CYB5A (evaluated by computerized algorithm through digital scanning: D-Dight, Menarini, Florence, Italy) had statistically significantly shorter survival (eg, median = 16.7 months, 95% confidence interval [CI] = 13.5 to 19.9; vs median = 24.8 months, 95% CI = 12.8 to 36.9; P =.02, two-sided log-rank test; n=82 radically resected PDACs), and multivariable analyses confirmed prognostic relevance. Moreover, we characterized a novel function to CYB5A, autophagy induction, concomitant with reduced proliferation and migration/invasion of PDAC cells. Network analysis of proautophagic pathways suggested CYB5A interaction

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with TRAF6, which was confirmed by TRAF6 downregulation after CYB5A reconstitution (−69% in SU.86.86-CYB5A+; P =.005, two-sided t test). CYB5A silencing had opposite effects, restoring TRAF6 expression and wound healing. In vivo studies showed that CYB5A induced autophagy while inhibiting tumor growth/metastasis and increasing survival (median = 57 days, 95% CI = 52 to 61; vs median = 44 days, 95% CI = 21 to 57; P = .03, two-sided log-rank test).

CONCLUSIONS: These results define CYB5A as a novel prognostic factor for PDAC that exerts its tumor-suppressor function through autophagy induction. Morerover, strategies aimed at restoring CYB5A activity, or targeted therapy inhibiting its deregulated downstream pathways, including TRAF6, may constitute a novel approach favouring cancer cell death while preventing potentially deleterious cross-talk between key oncogenic players in selected subgroups of PDAC patients.

S015 CA 19-9 RESPONSE TO NEOADJUVANT THERAPY PREDICTS OUTCOME IN PANCREATIC ADENOCARCINOMA Brian A Boone, MD, Jennifer Steve, BS, Melissa E Hogg, MD, Mazen S Zenati, MD, PhD, Amer H Zureikat, MD, Herbert J Zeh, MD, University of Pittsburgh, Pittsburgh, US

INTRODUCTION: Baseline Ca 19-9 is a useful prognostic marker in pancreatic ductal adenocarcinoma (PDA), however only a limited number of studies have examined the significance of a change in Ca 19-9 following neoadjuvant therapy.

METHODS: All patients receiving neoadjuvant therapy for PDA from 7/2010 to 2/2013 were retrospectively reviewed. Patients who had a pre-treatment Ca 19-9 that was normal (<33 U/mL) were excluded. Resection rate, R0 resection rate, need for venous resection and overall survival were correlated to Ca 19-9 response. Fischer exact test, Kaplan-Meier survival analysis and multivariate analysis using cox regression were used to evaluate data.

RESULTS: 79 patients were eligible for study (22 patients with resectable disease, 40 borderline resectable (BR) and 17 with locally advanced disease (LA)). A variety of chemotherapies +/- radiation were utilized during the study period (56% chemotherapy alone, 44% chemoradiation). The overall R0 resection rate was 67% (82% resectable, 70% BR, 41% LA). 56 patients (71%) had a decrease in Ca 19-9 with neoadjuvant treatment of >50%. For all patients, there was a trend towards a Ca 19-9 response of > 50% predicting R0 resection (OR 2.5, p=0.077). In BR patients, Ca 19-9 response of > 50% predicted R0 resection (OR 4.2, p=0.05). In BR patients that had an increase in Ca 19-9, 0 of 5 (0%) underwent R0 resection, while 80% of the remaining cohort had an R0 resection (p=0.001). The rate of complete pathologic response was 29% in patients who had a Ca 19-9 response of >90% versus 0% in the remaining patients (p<0.001). A Ca 19-9 response of >50% resulted in improved overall survival (28.0 vs. 11.1 months, p<0.0001, Figure 1). An increase in Ca 19-9 during treatment had an adverse effect on survival (10.2 vs. 28.0 months, p<0.0001). Ca 19-9 response of > 50% was an independent predictor of survival on multivariate analysis (p<0.0001, HR 0.26 [95% CI 0.13-0.55]).



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CONCLUSION: Ca 19-9 response to neoadjuvant therapy has prognostic value, predicting R0 resection rate and survival. This data supports the use of CA19-9 as an important biomarker of response to neoadjuvant therapy. Incorporation of this easily obtainable and rapid biomarker into future clinical trials may facilitate more rapid evaluation of novel regimens.

S016 DETECTION OF CLINICALLY RELEVANT GENETIC ALTERATIONS IN FINE NEEDLE ASPIRATES OF PANCREATIC CANCER IS POSSIBLE USING NEXT-GENERATION SEQUENCING Vicente Valero III, MD, Tyler J Saunders, BA, Matthew J Weiss, MD, John L Cameron, MD, Ralph H Hruban, MD, Joseph M Herman, MD, Christine A Iacobuzio-Donahue, MD, PhD, Christopher L Wolfgang, MD, PhD, The Johns Hopkins University School of Medicine, Department of Surgery, Baltimore, US

INTRODUCTION: A personalized approach to the treatment of pancreatic cancer that is based on genetic status depends on the tissue available for downstream molecular analysis. Fine needle aspiration (FNA) is the most commonly used method for obtaining tissue prior to surgical resection, or for patients in whom surgical resection is not indicated. Potentially limiting factors of FNA include the paucity of malignant cells within a fibroblast-rich stroma and tumor heterogeneity. Therefore, we sought to determine: the ability to confidently detect mutant alleles in low cellularity samples, the concordance between the FNA and the primary tumor and the feasibility of identifying driver mutations in clinical FNAs.

METHODS: We determined the ability to detect cancer-specific mutations in a wild-type stromal background in an in vitro model of Panc1 cells diluted into the fibroblast cell line, CAF-35. To demonstrate proof of principle, we mixed Panc1 with increasing cell ratios of CAF-35 (1:1, 1:10, 1:25, 1:50, 1:100, 1:200) to simulate the tissue heterogeneity seen in FNAs. To explore the impact of genetic heterogeneity

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on FNAs, we next established the mutational concordance between an FNA and its matched resected human adenocarcinoma tissue using next-generation sequencing by Ion Torrent PGM. Finally, 17 patient FNAs were sequenced using a targeted panel comprised of all exon coverage of 409 cancer related genes to identify driver, actionable and passenger mutations via FNA.

RESULTS: The limit of confident detection occurred at a 1:25 ratio of malignant to stromal cells for both the KRAS and TP53 mutant alleles corresponding to a hypothetical carcinoma with 4% neoplastic cellularity. Confident mutant detection was maintained at the 1:25 ratio when total cell count was varied with the lower limit of detection occurring at 25,000 total cells. The concordance rates between the FNA and tumor samples ranged from 83% to 100%, although there was 100% mutational concordance for driver genes in all samples. Sequencing of clinical FNAs revealed driver mutations of KRAS (93%), TP53 (53%), SMAD4 (40%) and CDKN2A (7%) genes. The total number of somatic mutations identified in this cohort was 80 (71 missense, 6 nonsense, 2 INDELs and 1 splice site) with a mean of 4.7 variants per patient. Other shared variants observed in these patients included SF3B1 (27%), ARID1A (20%), ATM (13%), TRIM33 (13%) and GRM8 (13%).

CONCLUSION: This is the first study to prove that confident genotyping of low cellularity FNA samples is possible and accurately detects the driver mutations in primary tumors. Furthermore, next generation sequencing can provide single base resolution for identification of clonal somatic variants found within the primary tumor. Moving forward, obtaining the genetic signature of an individuals pancreatic tumor will enable physicians to recommend personalized treatment plans to patients according to chemosensitivity, metastatic efficiency, perioperative outcome data and overall survival.

S017 NEW PLATFORMS FOR PDAC PRECLINICAL STUDIES: 3D TISSUE-ENGINEERED MODELS BASED ON PRIMARY CANCER CELLS AND SYNTHETIC SCAFFOLDS * Claudio Ricci, PhD, * Serena Danti, PhD, + Lorenzo Moroni, PhD, + Carlos Mota, PhD, ^ Stefania Moscato, PhD, * Delfo D’Alessandro, PhD, o Stefano Ugel, PhD, o Silvia Sartoris, PhD, o Vincenzo Bronte, MD, PhD, * Daniela Campani, MD, & Ugo Boggi, MD, * Niccola Funel, PhD; *Dept. of Surgical, Medical, Molecular Pathology and Emergency Medicine, University of Pisa, Pisa, Italy; +Tissue Regeneration Dept., University of Twente, Enschede, The Netherlands; ^ Dept. of Clinical Medicine, University of Pisa, Pisa, Italy; oDept. O, Pisa, IT

INTRODUCTION: Pancreatic Ductal Adenocarcinoma (PDAC) is a malignant neoplasm of epithelial origin which represents one of the major causes of death in the western world. At present, the Tumor Tissue Microenvironment (TME) is supposed to play a pivotal role on the aggressiveness of pancreatic epithelial tumor cells. Aim of this study was to investigate the interactions between PDAC cells (derived from patients who underwent surgical treatment) and different biocompatible scaffolds to generate new 3D in vitro models for TME studies.

METHODS: To create 3D cellular models, three scaffolds were fabricated with different polymers and techniques: polyvinyl alcohol/gelatin (PVA/G; weight



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composition ratio of 70/30) obtained via emulsion and freeze-drying; poly(ethylene oxide terephthalate)/poly(butylene terephthalate) (PEOT/PBT) produced via either compression molding and particle leaching (namely, CM) or electrospinning (namely, ES). Human epithelial primary cultures were derived from PDAC explants. Both tissues and derived cells were genetically characterized for K-ras and TP53. PDAC cells were seeded on the sterile scaffolds at a density of 1×104 cells/mm3 and cultured for 9 days in complete RMPI medium. Sample characterization included: cell viability (using the AlamarBlue assay), cell morphology [via scanning electron microscopy (SEM) and histology with H&E staining), expression of MMP9 and MMP2 proteins via Western Blot (WB) and immunohistochemistry (IHC).

RESULTS: At the endpoint cells were found to be viable in the scaffolds showing AlamarBlue reduction of 47.5% (PVA/G), 40.6% (PEOT/PBT_CM) and 45.1% (PEOT/PBT_ES). SEM analysis detected a good 3D colonization and a very strong cellular adhesion in all three models. The histologic analysis highlighted the formation of PDAC clusters showing a ductal-like morphology in both PVA/G and PEOT/PBT_CM models. Finally, in the 3D models, a higher expression of MMP9 and MMP2 proteins was observed with respect to 2D cell cultures.

DISCUSSION: From our findings, the development of 3D cancer tissue-engineered models using biocompatible scaffolds for cell growth seems to be feasible, versatile, low time consuming and representative of PDAC features. This platform could be used as a preliminary attempt before in vivo testing. In the close future, 3D models could be used to screen experimental pharmacological treatments for the modulation of different tumor proteins. Furthermore, in these 3D models an integration among different cellular types involved in PDAC microenvironment could be generated and be more representative of the human TME than the in vitro models used so far.

S018 BIOLUMINESCENT ORTHOTOPIC PANCREATIC-DUCTAL-ADENOCARCINOMA (PDAC) MOUSE MODELS DERIVED FROM PRIMARY PDAC CELLS AS A PLATFORM FOR THERAPEUTIC DISCOVERY Niccola Funel1,2, PhD, Elisa Giovannetti3, MD, PhD, Tonny Lagerweij4, PhD, Amir Avan3, PhD, Daniela Campani2, MD, Nelide De Lio1, MD, Vittorio Perrone1, MD, Dieter Fuchs5, PhD, Henk M Verheul3, PhD, Gerrit-Jan S Schuurhuis4, PhD, Godefridus J Peters3, PhD, Thomas Wurdinger4, MD, PhD, Ugo Boggi1, MD, 1Division of General and Transplant Surgery and 2Division of Surgical Pathology, University of Pisa, Pisa, Departments of 3Medical Oncology, and 4Neurosurgery & Pediatric Oncology/Hematology, VU University Medical Center; 5VisualSonics, Amsterdam, NL, Pisa, IT

BACKGROUND & AIM: Pancreatic ductal adenocarcinoma (PDAC) remains a major unsolved health problem. Most drugs that pass preclinical tests fail in these patients, emphasizing the need of improved preclinical models to test novel anticancer strategies. Early passages of primary PDAC cells may better mimic the genetic characteristics of the disease and might be better predictors of drug activity, including the standard treatment with gemcitabine. Recently, some authors developed primary models by implanting pieces of human PDACs subcutaneously into mice. However, subcutaneously implanted tumors may not

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optimally recapitulate many of the essential features of tumor growth in patients, such as the ability to metastasize. The aim of the present study was to develop orthotopic xenograft models using low passage primary PDAC cells injected in the pancreas of mice, preserving the genetic background and heterogeneity of human PDAC, while maintaining the macro- and micro-environmental interactions.

MATERIALS AND METHODS: We developed four orthotopic mouse models using primary human PDAC cells genetically engineered to express firefly- and Gaussia luciferase, simplifying the ability to monitor tumor growth and metastasis longitudinally in individual animals. Transduction efficiency was evaluated using fluorescence microscopy. Further imaging studies were performed with Magnetic Resonance Imaging and high-frequency ultrasound. In these models, we conducted detailed histopathologic and immunohistochemical analyses on paraffin-embedded pancreatic tissues and metastatic lesions in liver, lungs, and lymph nodes using a scanner for histopathology evaluation (D-SIght, Menarini, Florence, Italy). Genetic characteristics were compared with the originator tumors and primary tumor cells using array-based comparative genomic hybridization with the Agilent 4×180K platform, using frozen specimens obtained by laser microdissection.

RESULTS: Orthotopic human xenografts in these models recapitulated the phenotype of human PDACs, including hypovascular and hypoxic areas, as assessed by immunohistochemical analyses of CD31 and Carbonic Anhydrase IX, respectively. Pursuing genomic and immunohistochemical evidence revealed an increased copy number and overexpression of c-Met in one of the models. Therefore we examined the preclinical efficacy of c-Met inhibitors in vitro and in vivo. We found that crizotinib decreased tumor dimension, prolonged survival, and increased blood and tissue concentrations of gemcitabine.

Correspondingly, crizotinib reduced the activity of the gemcitabine catabolic enzyme cytidine deaminase (CDA), both in tissue specimens and blood samples. Since intact c-Met signaling is a critical factor in the protection against excessive generation of endogenous ROS, we demonstrated that a similar mechanism of post-transcriptional degradation induced by ROS was responsible for CDA reduction after exposure to crizotinib, resulting in the increased stabilization of gemcitabine.

CONCLUSIONS: Our more readily imaged orthotopic PDAC models displayed genetic, histopathologic, and metastatic features similar to their human tumors of origin. Moreover, their use pointed to c-Met as a candidate therapeutic target in PDAC and highlighted crizotinib and gemcitabine as a synergistic combination of drugs warranting clinical evaluation for PDAC treatment.

S019 COUNTERACTING CANCER CELL SURVIVAL STRATEGY: SENSITIZATION OF PANCREATIC CANCER CELLS TO TRAIL INDUCED CELL DEATH BY JAK2/STAT3 PATHWAY INHIBITION BY PREVENTING DEATH RECEPTOR DOWNREGULATION Kaustav Majumder, MD, Steve Skube, MD, Rohit Chugh, MD, Sulagna Banerjee, PhD, Ashok Saluja, PhD, Vikas Dudeja, MD, University of Minnesota, Minneapolis, US

INTRODUCTION: TRAIL (Tumor Necrosis Factor-Related Apoptosis Inducing Ligand) is emerging as a promising anti-cancer therapy by virtue of its strong



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anti-tumor activity against a wide range of cancer cells and minimal toxicity to normal cells. Unfortunately, pancreatic cancer is resistant to TRAIL. TRAIL binds to Death Receptors (DR4 and DR5) and forms DISC (Death inducing signaling complex) that further activates downstream caspases leading to cell death via apoptosis. TRAIL receptor down-regulation by virtue of endocytosis has been shown to be one of the mechanisms of TRAIL resistance in cancer cells. The aim of the current study was to evaluate the combination of TRAIL and JAK-2 down-regulation against pancreatic cancer as well as to examine the mechanism for the proposed synergism.

METHODS: Highly aggressive metastatic pancreatic cancer cell lines (S2013, S2VP10) and Hepatocellular cell lines (HUH-7) were treated with JAK-2 inhibitor FLLL-31 (0-5µM), TRAIL (0-40ng/ml) and a combination of JAK-2 inhibitors and TRAIL. The effect on viability (MTT) and parameters of apoptosis (Annexin V, Caspase 3, 8 and 9 activation) was measured. Flow Cytometry was used to evaluate cell surface expression of death receptors. Immuno-precipitation was used to assess formation of DISC complex.

RESULTS: TRAIL in itself was ineffective in inducing cell death in pancreatic cancer cells but combination of TRAIL and JAK2 inhibitor FLLL-31 induced marked decrease in viability and increase in the markers of apoptosis (table). TRAIL treatment led to down-regulation of both DR4 and DR5 receptors in pancreatic cancer cell lines S2VP10 and S2013. Intriguingly, in presence of JAK2/STAT3 inhibitor, TRAIL treatment did not downregulate death receptors and was associated with increased DISC complex formation and increased activation of Caspase-8 [DR5 receptor level, expressed as % of levels in untreated cells (mean ± SEM) - S2013: TRAIL 20ng/ml 62±12.9%, TRAIL 20ng/ml + FLLL-31 100.2±15; S2VP10: TRAIL 20ng/ml 46.4±18.7%, TRAIL 20ng/ml + FLLL-31 101±8.8.]

CONCLUSION: Inhibition of JAK-2/STAT3 pathway sensitizes pancreatic cancer cells to TRAIL induced apoptosis and cell death via inhibition of down-regulation of DR4 and DR5. This leads to increased availability of death receptors and increased formation of DISC and augmentation of downstream apoptotic pathway. Combination of JAK-2/STAT3 silencing and TRAIL has immense potential to emerge as novel therapeutic strategy against pancreatic cancer.

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S020 TOTAL PANCREATECTOMY WITH ISLET AUTOTRANSPLANTATION FOR CHRONIC PANCREATITIS: THE PRICE PATIENTS PAY FOR IMPROVEMENTS IN QUALITY OF LIFE Katherine Morgan, MD, David B Adams, MD, Stefanie M Owczarski, PAC, Hongjun Wang, PhD, Wendy Balliet, PhD, Jeffrey Borckardt, PhD, Medical University of South Carolina, Charleston, US

BACKGROUND: For selected patients with debilitating pain from chronic pancreatitis total pancreatectomy with islet autotransplantation (TPIAT) has been undertaken with recently increased enthusiasm. Safety and efficacy, i.e. “patient-centered cost”, of this radical procedure has not been well assessed previously.

METHODS: A retrospective review of a prospectively collected database of patients undergoing TPIAT was undertaken. Perioperative morbidity, quality of life (QOL, SF-12), and insulin use were assessed preoperatively and at 12 and 24 months postoperatively.

RESULTS: One hundred twenty patients (93 women, mean age 41, mean BMI 26.2) underwent TPIAT. Duration of pancreatitis prior to TPIAT averaged 7.6 years (0.5-40). Mean operative time was 237 minutes (75-395), EBL was 618 cc (50-7800), and median islet equivalents transplanted were 256,470 (969-1,168,725), or 3640 IEQ/kg (14-16010). Average length of hospitalization was 12 days. Twelve patients required reoperation in the 30-day post-operative period (10%). Postoperative morbidity overall was 68% and 23% of patients had a complication requiring intervention (Clavien-Dindo IIIa or greater). Perioperative mortality was 1.6%. Five patients (4%) died in the follow-up period. Eighty-five patients were available for at least 12 month follow-up. Physical QOL went from mean 27 preoperatively to 35 and 33 at 12 and 24 months (p=0.001, 0.003) and mental health QOL went from 38 to 42 and 41 (p=0.02, 0.2). Insulin independence was achieved in 26% and 29% at 12 and 24 months respectively.

CONCLUSION: Quality of life is significantly improved in patients who undergo TPIAT for chronic pancreatitis, but with notable costs in perioperative morbidity and diabetes. Improvements in physical and mental QOL are sustained up to two years after surgery.

S021 COST-EFFECTIVENESS OF TOTAL PANCREATECTOMY WITH ISLET CELL AUTOTRANSPLANTATION FOR THE TREATMENT OF SMALL DUCT CHRONIC PANCREATITIS Gregory C Wilson, MD, Daniel E Abbott, MD, Daniel P Schauer, MD, MSc, Mark H Eckman, MD, MS, Syed A Ahmad, MD, University of Cincinnati Medical Center, Cincinnati, US

INTRODUCTION: Total pancreatectomy and islet cell autotransplantation (TPIAT) has gained popularity for managing chronic pancreatitis (CP), but a cost-benefit assessment has not been scientifically performed. We hypothesized that TPIAT decreases long-term resource utilization and improves quality-of-life, justifying the initial costs and risks of the procedure.

METHODS: From 1999-2013, 46 patients with small duct CP and detailed treatment and outcomes data in the perioperative period (12 months before and



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after TPIAT) were analyzed. These data populated a Markov model comparing ongoing medical management versus TPIAT for small duct CP. The surgery cohort included perioperative mortality and complication rates, while CT imaging, insulin use, morphine equivalent (MEQ) and endoscopic procedure (EGD, EUS, ERCP) and readmissions were used in both surgical and medical cohorts. Survival (quality adjusted life years, QALY) and cost (based on Medicare payment, 2013 US$) were discounted at 3% per year.

RESULTS: Median patient age was 36 years (range = 15-61) with a predominance of females (n=29, 63%). The etiologies of CP were primarily idiopathic (n=30, 65%) followed by genetic (n=12, 26%). In the 12 months prior to TPIAT (medical management cohort), annual mean per patient hospital admissions were 1.6 (range = 0-11), endoscopic procedures 1.3 (range = 0-6), and imaging (CT/MRI) 1.3 (range = 0-4). In the surgical cohort there were no perioperative deaths, with complication and 30-day readmission rates of 41% and 37%, respectively. 1 year after TPIAT, annual mean per patient admissions, endoscopic procedures and imaging had decreased to 0.9 (range = 0-4), 0.4 (range = 0-2) and 0.9 (range 0-5), respectively. Furthermore, monthly narcotic use in the surgical cohort decreased from 138 to 37 MEQ (p=0.012). Cost and survival for TPIAT versus continued medical management were $153,575/14.9 QALYs and $196,042/12.8 QALYs, respectively. Sensitivity analyses with variable perioperative mortality rates, quality of life adjustment and TPIAT payment did not substantially change the cost-effectiveness analysis.

CONCLUSIONS: In patients with refractory small duct CP, TPIAT is associated with both decreased cost and increased quality-adjusted survival. Because TPIAT is a cost-effective treatment for small duct pancreatitis, tertiary care centers should look for opportunities to increase the use of TPIAT, and insurers should more enthusiastically embrace its use.

S022 HIGH READMISSION RATES FOLLOWING SURGERY FOR CHRONIC PANCREATITIS A V Fisher, J M Sutton, MD, G C Wilson, MD, D J Hanseman, D E Abbott, MD, M T Smith, MD, N Schmulewitz, MD, K A Choe, MD, J Wang, MD, PhD, J J Sussman, MD, S A Ahmad, MD, University of Cincinnati, Cincinnati, US

INTRODUCTION: Readmission after complex gastrointestinal surgery

is a frequent occurrence which burdens the healthcare system and leads to increased cost. Recent studies have demonstrated 30-day and 90-day readmission rates of 15% and 19%, respectively, following pancreaticoduodenectomy (PD) for all indications. Given the psychosocial issues often associated with chronic pancreatitis, we hypothesized that readmission rates following surgery for chronic pancreatitis would be higher than previously reported for PD.

METHODS: We retrospectively reviewed patients undergoing surgery for head-predominant chronic pancreatitis at a single institution between 2001 and 2013. Patients in this cohort underwent PD, Berne, Beger, or Frey procedures. Readmission to a primary or secondary hospital was evaluated at both 30 days and 90 days following discharge. Multivariate logistical regression analysis was

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performed to identify patient demographics, comorbidities, peri-operative factors, and complications associated with readmission.

RESULTS: The records of 111 patients were evaluated, of which 69 (62%) underwent duodenal sparing head resection (DSHR; Berne, Beger, Frey), and the remaining 42 (38%) underwent PD. Within the DSHR arm, readmission rates at 30 days and 90 days were 30.4% and 43.5% respectively. Due to multiple readmissions for several patients, there were a total of 57 readmissions within 90 days. Within the PD arm, readmission rates were similar with 33.3% at 30 days, 40.5% at 90 days, and 34 total readmissions within 90 days. The most common reasons for readmission in both cohorts were pain control, infectious complications, and recurrent pancreatitis. On multivariate analysis of the entire cohort, wound infection during initial hospital stay was a predictor of readmission at both 30 and 90 days (p=0.003). Within 90 days following discharge, factors associated with readmission included dehydration/malnutrition (p=0.047), and intractable pain (p=0.023). Factors not associated with readmission included age, Charlson co-morbidity index, etiology of pancreatitis, duration of disease, type of operation, operative time or blood loss, presence of a post-operative pancreatic fistula, transfusion requirements, respiratory complications (pneumonia, pleural effusion, respiratory failure/insufficiency), and length of initial hospital stay.

CONCLUSIONS: To our knowledge, our data represents the first report demonstrating very high readmission rates following surgery for chronic pancreatitis, more than double the previously reported rates following PD for all causes. This cohort of patients requires significant discharge planning focused on pain control, nutritional optimization, and close post-operative monitoring. This study may serve as a benchmark for further investigation into readmission rates following the surgical treatment of chronic pancreatitis.

S023 PANCREATICODUODENECTOMY FOR CHRONIC PANCREATITIS: A LONG-TERM FOLLOW-UP Kristopher P Croome, MD, David M Nagorney, MD, Mark J Truty, MD, Kaye Reid-Lombardo, MD, Florencia G Que, MD, Michael L Kendrick, MD, Michael B Farnell, MD, Mayo Clinic - Rochester, Rochester, US

BACKGROUND: Over the last 30 years significant developments in the management of chronic pancreatitis (CP) have occurred due to refinements in surgical technique, improvements in diagnostic imaging and advancement in the use of endoscopic therapies. This has led some authors to question the role of pancreaticoduodenenctomy (PD) in chronic pancreatitis. The present study aimed to examine the long-term outcomes of PD for CP as well as assess how practice has changed over time.

METHODS: All patients who underwent PD for CP between the dates of January 1976 and July 2013 were identified. Patient records were reviewed. Patients were contacted for response to a follow-up questionnaire and SF-12 Quality of Life Health Survey administration. Patients were divided in 2 eras: Cohort 1 (1976-1999) and Cohort 2 (2000-2013).



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RESULTS: A total of 166 patients were identified (Cohort 1 (N=105) and Cohort 2 (N=61)). Median time from presentation until surgery was significantly longer in cohort 2 (2.09 years (2months - 23 years)) compared to cohort 1 (1.13 years (1month - 39 years)) (p=0.017). A higher proportion of patients in Cohort 2 (98%) had intractable pain prior to surgery than in cohort 1 (82%) (p=0.002). Prior to PD a higher proportion of patients in cohort 2 had undergone endoscopic stenting compared to cohort 1, 67% and 10% respectively (p<0.001). A higher proportion of patients had also undergone celiac plexus block 15% and 5% (p=0.026). Operative mortality was not significantly different between cohort 2 (0%) and cohort 1 (3%) (p=0.18). Median follow-up for all survey respondents was 17.8 years. On the SF-12, mean physical component score (PCS) was 48.9±8.7 and mental component score (MCS) was 56.8±5.22. Patients were not significantly different on the PCS (p=0.65) and significantly better on the MCS (p=0.004) than the general US population. Mean pain score out of 10 was significantly lower after surgery 1.3±2.6 than before surgery 8.0±3.8 (p<0.001). At time of last follow-up, diabetes had developed in 38% of patients who were not diabetic prior to surgery.

CONCLUSION: Although practice has changed so that patients have a longer time from presentation until surgery as less invasive techniques are attempted, PD appears to provide effective long-term pain relief and quality of life in patients who continue to have intractable pain after other interventions have failed.

S024 RISK OF RECURRENT PANCREATITIS AND PROGRESSION TO CHRONIC PANCREATITIS AFTER ACUTE PANCREATITIS Usama Ahmed Ali, MD, MSc, Yama Issa, MD, Julia C Hagenaars, MD, Olaf J Bakker, MD, Harry van Goor, MD, PhD, Vincent B Nieuwenhuijs, MD, PhD, Thomas L Bollen, MD, Bert van Ramshorst, MD, PhD, Ben J Witteman, MD, PhD, Menno A Brink, MD, PhD, Alexander F Schaapherder, MD, PhD, Cornelis H Dejong, MD, PhD, Marcel B Spanier, MD, PhD, Joos Heisterkamp, MD, PhD, Erwin van der Harst, Casper H van Eijck, MD, PhD, Marc G Besselink, MD, PhD, Hein G Gooszen, MD, PhD, Hjalmar C van Santvoort, MD, PhD, Marja A Boermeester, MD, PhD, Department of Surgery, Academic Medical Center, Amsterdam, Utrecht, NL

BACKGROUND & AIMS: Most patients with acute pancreatitis (AP) achieve complete recovery, but certain patients may develop recurrences and even progress to chronic pancreatitis (CP). This study aims to evaluate these events and their risk factors.

METHODS: A cross-sectional survey and retrospective review of an initially prospectively collected cohort of patients with a first episode of acute pancreatitis was performed. Primary endpoints were development of recurrent pancreatitis (RP) and progression to CP. Risk factors for RP and CP were evaluated using regression analysis, and cumulative risk was assessed using Kaplan-Meijer analysis.

RESULTS: We included 670 patients that survived a first acute pancreatitis episode. Median follow-up was 5 years. RP and CP were observed in 124 (19%) and 42 (6.3%) patients, respectively. Rates of RP were in 13.0%, 24.8% and 25.8%

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of patients with biliary, alcoholic and idiopathic/other etiology, respectively. Progression to CP occurred in 2.3%, 15.0% and 7.4% for these etiologies, respectively. Etiology, smoking and pancreatic necrosis were independent risk factors for both RP and CP. APACHE-II score was an additional independent risk factor for RP. Cumulative risk for RP over 5 years was the highest among smokers (about 42% over 5 years). A cumulative risk of progression to CP of about 15% was observed in patients with alcohol etiology and in smoking patients. When both an alcoholic etiology and smoking were present the cumulative risk increased to 30%.

CONCLUSIONS: The risk of developing RP and CP is highly dependent on risk factors. Predominantly smoking is an independent risk factor for RP. For CP, the combination of alcohol and smoking results in the highest cumulative risk. The strong association of pancreatic necrosis with RP and CP provides support for the ‘necrosis-fibrosis-sequence’ theory for disease progression.

S025 SEVERE ACUTE PANCREATITIS: USING A MULTIDISCIPLINARY PERCUTANEOUS DRAINAGE PROTOCOL THE MAIN PREDICTOR OF HOSPITAL LENGTH OF STAY IS AMYLASE OR BACTERIA IN THE PERCUTANEOUS ASPIRATE M Sugimoto, MD, G S Flint, C J Boyce, J C Kirkham, L Nesbit, S M Schutz, J T Witte, M L Lloyd, J G Barton, T J Harris, D P Sonntag, S M Carr, B D Nelson, D A Bell, L W Traverso, Departments of Radiology, Gastroenterology, and Surgery, St. Luke’s Health Care System, Boise, US

INTRODUCTION: In addition to critical organ support many patients with severe acute pancreatitis (SAP) will require drainage followed by nutritional support and antibiotics. How important is drainage? A risk analysis of clinical parameters for the outcomes of hospital length of stay (LOS) or mortality may provide an answer.

METHODS: During a 39 month period 98 patients were hospitalized with SAP – defined as having clinical symptoms of pancreatitis, pancreatitis confirmed by contrast enhanced CT, and the presence of one of the following CT findings: peripancreatic fluid collections, pseudocyst, or lack of parenchymal contrast enhancement (necrosis). Every CT scan for each patient was scored for severity by 2 radiologists reaching consensus using the modified CT severity index (CTSI, Mortele et al., AJR 2004;183:1261). The maximum CTSI was recorded. Only symptomatic cases were treated with drainage based on a standardized multidisciplinary approach beginning with a percutaneous drainage protocol with frequent CT/drain exchanges and escalating to open necrosectomy for lack of progress. Main outcomes were LOS and mortality. The clinical course was analyzed for those risk factors associated with increased LOS.

RESULTS: The median CTSI was 6 for all patients (n=98) and 8 for percutaneous drainage cases (n=41). The median LOS for all cases = 13 days and for percutaneous drainage cases = 24 days. In this consecutive patient cohort, in-hospital mortality was zero. Open necrosectomy was not required. Univariate analysis showed a significant relationship with a longer LOS ≥ 14 days to the following clinical parameters: older age (OR = 1.032, P = 0.019), systemic inflammatory response syndrome (OR = 2.482, P =0.028), organ failure (OR = 6.622, P = 0.019), necrosis



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(OR = 2.700, P = 0.018), and presence of high amylase (more than 1000) or bacteria in the initial drainage fluid (OR = 10.127, P <0.001). Multivariate analysis showed age (OR = 1.032, P = 0.038) and presence of high amylase or bacteria in the drainage fluid (OR = 7.416, P = 0.002) as independent risk factors for increased LOS.

CONCLUSION: In symptomatic patients with SAP and a CTSI of 8, a standardized multidisciplinary percutaneous drainage protocol was able to accomplish a zero in-hospital mortality with a median LOS of 24 days. Among all measured parameters associated with SAP the strongest OR for increased LOS was the presence of amylase or bacteria in the aspirate at the time of initial percutaneous drainage. This finding emphasizes the importance of continuous adequate drainage. In our institution this was accomplished using a standardized protocol directing frequent catheter exchanges resulting in no hospital mortality.

S026 SURGICAL RESECTION PROVIDES A SIGNIFICANT OVERALL SURVIVAL BENEFIT FOR PATIENTS WITH SMALL PANCREATIC NEUROENDOCRINE TUMORS Susan M Sharpe*, MD, Haejin In*, MD, MPH, MBA, David P Winchester ,̀ MD, Mark S Talamonti^, MD, Marshall S Baker^, MD, MBA, *Department of General Surgery, University of Chicago, Chicago, IL; ^Department of General Surgery, NorthShore University HealthSystems, Evanston, IL; `American College of Surgeons, Chicago, IL, Chicago, US

INTRODUCTION/BACKGROUND: Pancreatic neuroendocrine tumors (PNETs) have a widely variable potential for malignant behavior. Most series examining the efficacy of surgical resection of these tumors are underpowered, single institutional, retrospective studies. There continues to be controversy regarding the optimal management of incidentally discovered small (<= 2 cm) non-functioning PNETs. We evaluated the sub-population of small, non-functional PNETs in the National Cancer Data Base (NCDB) to determine if an aggressive surgical approach provides a significant survival advantage over observation.

METHODS: The National Cancer Data Base was queried to identify all patients with PNETs <= 2 cm in size treated between 2003 and 2011. Patients with metastatic disease at the time of presentation and those with unknown histologic grade were excluded. Kaplan-Meier analysis, stratified by histologic grade and treatment type, was used to evaluate the difference in 5-year overall survival (OS) between patients who received surgery and those who did not. Multivariable Cox regression was used to determine the relative importance of surgical intervention in overall survival.

RESULTS: 749 patients met inclusion criteria. 93.2% underwent surgery and 6.8% were managed with observation alone. 24.7% were size 0-1 cm and 75.3% were 1.1-2 cm. There were no significant differences between patients in the surgical and observation cohort with regard to tumor size, tumor location, or comorbid disease characteristics. A greater percentage of patients in the observation cohort had moderately or poorly differentiated tumors than did patients in the surgical cohort (37.3% vs. 11.3%, p<0.05). Five-year OS was 89.6% for patients

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who underwent surgery and 40.1% for those who did not (p<0.0001). Variables included in the final multivariate Cox model were selected by backwards selection and included: age, Charlson score, tumor location, histologic grade, and treatment (surgery vs. observation). When controlling for Charlson score, age, and tumor location, observation without surgical resection (OR 4.94, 95% CI [2.79, 8.76]) and poorly differentiated histology (OR 8.15, 95% CI [4.47, 14.85]) were independently associated with a significant increase in the risk of death (p<0.0001). Lymph node positivity and tumor size were not associated with an increased risk of death.

DISCUSSION/CONCLUSION: In patients with localized, non-functional pancreatic neuroendocrine tumors 2 cm in size or smaller, surgical resection provides a significant overall survival advantage over observation. This benefit is independent of patient age, co-morbid status, and histologic grade of the tumor.

S027 RISK OF MALIGNANCY IN RESECTED NONFUNCTIONING PANCREATIC NEUROENDOCRINE TUMORS Michael J Ferrara, MS, Michael B Farnell, Kristopher P Croome, Michael L Kendrick, Mayo Clinic Rochester, Rochester, US

BACKGROUND: Surgical resection is considered for nonfunctioning pancreatic neuroendocrine tumors (nPNET) due to their malignant potential. Tumor size is a known predictor of malignancy although the size warranting resection continues to be debated. The aim of this study was to evaluate the risk of malignancy based on clinicopathologic factors in patients undergoing resection of nPNET.



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METHODS: Retrospective review of all patients undergoing pancreatic resection of sporadic nPNET at a single tertiary center from 2004 through 2012. Patients with known metastasis or those with associated familial syndromes were excluded. Preoperative imaging (MRI or CT) was reviewed to assess for features suspicious for malignancy. Histopathology of resected specimens was reviewed for evidence of malignancy (invasion or lymph node metastases). Median postoperative follow-up was 32 months.

RESULTS: Of 169 patients, median tumor size was 2.7 cm (range 0.6 cm – 16.5 cm). Malignancy was identified in 64 (38%) patients. Increasing tumor size was associated with malignancy on logistic regression (p<0.001). Occurrence of malignancy increased with tumor size: <1cm (0%), 1-1.9cm (22%), 2-3.9cm (32%), ≥4cm (62%). Malignancy was also more common in patients with suspicious features on imaging (58% vs. 23%, p<0.001). Occurrence of lymph node metastases increased with tumor size: <1cm (0%), 1-1.9cm (12%), 2-3.9cm (27%), 4cm (41%). Prediction of malignancy was investigated by tumor size. Area under the curve for tumor size was 0.73 with an optimal cutoff of 2.6cm. Tumor recurrence was identified in 21 (12%) patients, including 5 patients with no evidence of malignancy at initial resection. Patients with lymph node metastases were more likely to have tumor recurrence (28% vs. 9%, p=0.03).

CONCLUSIONS: Risk of malignancy in sporadic nPNET is significant even in small tumors. Malignancy was identified in 22% of tumors between 1 and 1.9cm with lymph node metastasis in 12%. These findings should prompt consideration of resection for tumors greater than 1 cm and suggest that resection with regional lymphadenectomy should be favored over enucleation.

S028 AN INVESTIGATION OF THE UTILITY OF KI-67 EXPRESSION IN PANCREATIC NEUROENDOCRINE TUMOUR FINE NEEDLE ASPIRATION SAMPLES Nigel B Jamieson, MD, PhD, Lewis Morrison, BSc, Ross Carter, MD, Euan J Dickson, MD, Colin J Mckay, MD, Fraser Duthie, MD, Academic Unit of Surgery and West of Scotland Pancreatic Unit, Glasgow Royal Infirmary, G31 2ER, Scotland, UK., Glasgow, GB

BACKGROUND: Pancreatic endocrine tumors (PETs) are uncommon and represent 1% to 2% of all pancreatic neoplasms. Endoscopic ultrasonography (EUS) in combination with fine needle aspirate (FNA) is a highly accurate method for the preoperative diagnosis and staging of pancreatic mass lesions. Despite the utility of Ki-67 proliferative index of resected PETs for determining prognosis postoperatively, the role of preoperative FNA sample derived Ki-67 expression levels have yet not been investigated in depth.

AIMS: To assess the correlation between Ki-67 levels within PETs from preoperative FNA and surgical resection specimens.

METHODS: Patients with PET tumors managed at the West of Scotland Pancreatic Unit with full clinicopathological follow-up data were identified from a prospective maintained database from 1999 to 2012. For this study, samples were only included if adequate diagnostic preoperative cytology samples and subsequent surgical resection were available. Immunocytochemical Ki-67 expression levels

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were assessed using validated manual counting techniques in both cytology and resection specimens. A comparison of cytology and corresponding resection Ki-67 levels were performed.

RESULTS: 59 patients with PETs underwent resection during the study period. Appropriate tissue was available from 22 patients. In these, significant correlation was found between preoperative cytology and resection Ki-67 scores (Spearman’s Rho = 0.6, P = 0.01). An elevated Ki-67 level was an independent predictor of poor survival following resection (Hazard Ratio = 2.5, P=0.01). More importantly, an elevated Ki-67 expression in preoperative EUS-FNA cytology specimens was significantly associated with a reduced overall survival compared to those patients with tumors expressing a low Ki-67 level (P=0.008, Log-rank).

CONCLUSION: Our study shows that cytological derived Ki-67 levels match closely with those measured on resected specimens suggesting it can be a reliable predictor of the behavior and prognosis of PETs. This data has important implications for the staging and management of patients with PETs particularly those with borderline fitness who would be best served by a non-operative approach.

S029 THE GASTRINOMA TRIANGLE REVISITED: DUODENAL WALL GASTRINOMA AND PANCREATIC GASTRINOMA LOCATIONS PREDICT BIOLOGICAL BEHAVIOR AND LONGEVITY Sam G Pappas, MD, Kara M Doffek, BS, Kathleen K Chrisitans, MD, Edward J Quebbeman, MD, Douglas B Evans, MD, Stuart D Wilson, MD, Loyola University Medical Center; Medical College of Wisconsin, Maywood, US

INTRODUCTION: This prospective 51 year observational study investigates the biological behavior and longevity of sporadic gastrinomas (Zollinger-Ellison’s syndrome) with specific reference to tumor location and longevity. Passaro’s studies of the gastrinoma triangle suggest 2 types of gastrinomas based on origin of location. Fendrich’s recent investigation with molecular markers further explain a possible different genetic background between duodenal wall gastrinoma (DWG) and pancreatic gastrinomas (PG).

METHODS: The study cohort consisted of 41 consecutive patients with sporadic gastrinomas followed in the Clinical Research Center (CRC) and/or who underwent operations over a 51 year period 1962- 2012. A diagnosis of sporadic form of Zollinger-Ellison (ZE) syndrome was established in all patients.

RESULTS: Patients were divided into 2 groups based on tumor location. Thirty-five patients with extrapancreatic gastrinoma found in the duodenal wall and/or paraduodenal lymph nodes were assigned DWG group. Five patients with primary pancreatic gastrinoma were assigned PG group. One patient with a primary gastrinoma in the gastric antral wall was considered separately. Clinical presentation (i.e. symptoms, ulcers, gastric acid, gastrin) were similar in DWG and PG groups. Total gastrectomy (26 patients) was most common in the era (1962-1979) prior to advent of effective acid suppression medications. Subsequent operations have attempted to cure by excising DWG and/or paraduodenal lymph nodes. Overall mean survival for 35 DWG patients has been 16.5 years vs. 2.3 years for 5 PG patients(p<.05). Remarkably none of the DWG patients died from



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tumor progression or developed liver metastasis even when operation was not curative and hypergastrinemia persisted whereas all 5 PG patients died early with progressing liver metastasis.

DISCUSSION: This 51 year observational study supports the concept that DWG and PG are distinct clinical entities. The biological behavior of these 2 different gastrinomas portends different outcomes. PG tumors metastasize early to the liver and patients are short-lived. Whereas in DWG patients liver metastasis were not observed and there were no deaths from tumor progression . Management of DWG and PG entities should be different.

S030 PATTERNS OF PRACTICE AND SURVIVAL AMONG PATIENTS WITH NON-METASTATIC PANCREATIC NEUROENDOCRINE TUMORS UNDER 2 CM Jan Franko, MD, PhD, Charles D Goldman, MD, Mercy Medical Center DSM, Des Moines, US

BACKGROUND: Discrepant evidence is available for treatment of small non-functional pancreatic endocrine tumors (NF-PET). We examined practice patterns and overall survival among patients with NF-PET and tumor size 2 cm and smaller.

METHODS: The NCDB Participant Use Data File (PUF) for pancreas covering 1998-2011 was queried for clinical characteristics, demographic, treatment and outcome data for all cases coded as NF-PET. Survival analysis was performed for patients diagnosed 1998-2006 to allow at least five years of follow-up.

RESULTS: Data on initial resection versus observation were available on 6,689 cases of non-metastatic NF-PET. 270 (4%) of small non-metastatic NF-PETs were initially observed. This proportion was 14% among those with stage I-II disease. There was no trend in resection and observation rates over the study period.

Initial observation rather then resection among non-metastatic patients was to some extent predicted by multinomial logistic regression (pseudo R2=0.276, p<0.001). Observation was more common with younger age, pancreatic head location, and tumors ≤2cm, but not influenced by modified Charlson-Deyo comorbidity index.

Among resected non-metastatic NF-PETs sized ≤2 cm 72.8% were node-negative, whereas 27.2% were node-positive. Higher proportion of node-positive disease was observed among corresponding patients with tumor size over 2 cm (49.5% node-positive, p<0.001).

Survival among non-metastatic small PET was better among those resected (p<0.001) even when analysis was restricted to those with clearly resectable disease (stage I-II, p=0.014). Cox model demonstrated that age, resection rather then observation (HR=0.25), nodal status (HR=1.47), and size >2 cm (HR=1.55) were predictive of survival, but not comorbidity and tumor location (head vs. body/tail).

CONCLUSION: A small proportion of non-metastatic NF-PET is not initially resected, but observed. Clinical characteristics explain only 27% variability in decision to operates versus observe. Resection of even small NF-PETs measuring 2 cm and less is associated with improved survival. This analysis supports resection of all NF-PETs, including those smaller than 2 cm.

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S031 RE-CLASSIFICATION OF COMBINED-TYPE IPMNS ALLOWS FOR A BETTER DEFINITION OF TWO DISEASE ENTITIES Giovanni Marchegiani, MD, Mari Mino-Kenudson, MD, Klaus Sahora, MD, Cristina Ferrone, MD, Sarah Thayer, MD, Andrew L Warshaw, MD, Keith D Lillemoe, MD, Carlos Fernandez-del Castillo, MD, Massachusetts General Hospital - Harvard Medical School, Cambridge, US

BACKGROUND / AIM: Malignant potential of IPMNs is associated with involvement of the main pancreatic duct (MPD). Mixed-type or combined IPMNs have been historically categorized together with main duct tumors. However, combined IPMNs encompass a spectrum which differs in terms of extent of MPD involvement. We sought to re-classify combined IPMNs to better define groups that may diverge in pathological features and biological behavior.

METHODS: Slide re-classification by a single pancreatic pathologist of all IPMNs operated between 1990 and 2013 at the MGH. IPMNs were divided into lesions with predominant involvement of the MPD (pred-MD) and into those with predominant involvement of the branch ducts (pred-Bd).

RESULTS: Out of 421 patients who underwent surgery for IPMN, 386 patients had enough material for re-review. 176 (46%) were pred-MD and 210 (54%) pred-Bd. Median age was 67 in both groups; male-to-female ratio was 1.1:1 in pred-MD and 1:1.3 in pred-Bd (P=0.02). Pred-MD were significantly more likely to be smokers, diabetic, jaundiced and to have a history of pancreatitis, weight loss and an elevated CA 19.9 (all P<0.05). Pred-MD were of the intestinal and gastric epithelial subtype in 48% and 34% of cases, respectively, while in pred-Bd these frequencies were 14% and 80% (P<0.001). 72% of pred-MD had high-grade dysplasia or more, whereas 79% of pred-Bd were either low- or intermediate-grade (P<0.001). Invasive carcinoma was found in 39% of pred-MD compared to only 5% of pred-Bd (P<0.001); the latter were mostly tubular (83%), whereas pred-MD were spread between colloid (31%), tubular (59%) and oncocytic (10%) (P=0.08). Distinct PDAC was present in 2.8% of pred-MD and in 6.1% of pred-Bd (P=0.1)

Median follow-up was 90 months and 5-year overall survival 77%. 5-year disease-specific survival was 83% and 96% for the pred-MD and pred-Bd, respectively (P=0.002). For invasive cancers, 5-year DSS was 64% for the pred-MD and 41% for the pred-Bd (P=0.2). At 10 years overall recurrence rates were 25% and 17% for pred-MD and pred-Bd respectively (P=0.08), but for invasive tumors they were 48% in pred MD and 81% in pred Bd (P=0.04).

CONCLUSIONS: Re-classification of combined IPMN based on the actual extent of MPD involvement identifies two different entities in terms of epidemiology, biology and outcome. Pred-MD are more symptomatic and malignant than pred-Bd, and are associated with a worse prognosis. However, invasive pred-BD recurs more often and tends to have a worse disease specific survival than invasive pred-MD.



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S032 CLINICAL VALIDATION OF NEW INTERNATIONAL CONSENSUS GUIDELINES FOR THE RESECTION OF BRANCH DUCT TYPE INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS (BD-IPMN) Jin-Young Jang, Selyeong Lee, Mee Joo Kang, Taesung Park, Kyoung Bun Lee, Wooil Kwon, Ye Rim Chang, Seung Yeoun Lee, Sun-Whe Kim, 1Department of Surgery and Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea 2Department of Statistics, Seoul National University College of Natural Sciences, Seoul, Korea 3Department of Pathology, Seoul National Univ, Seoul, KR

BACKGROUND: Despite new consensus guidelines, classifications of intraductal papillary mucinous neoplasm(BD-IPMN) remain ambiguous, especially for mixed type, and factors predicting malignancy remain unclear. The aim of this study was to evaluate the clinical usefulness of each factor predicting malignancy in the new consensus guidelines for resection of branch duct type (BD-IPMN) and to validate new guideline comparing with previous one.

METHODS: The sensitivity, specificity, balanced accuracy and area under the receiver operating characteristic (ROC) curve for the first and second consensus guidelines were compared. The statistical importance of each variable was analyzed in a prospectively collected database of 350 patients with biopsy proven BD-IPMN.

RESULTS: Random Forest models showed that the sensitivity, specificity, and area under the ROC curve (AUC) were 0.639, 0.822, and 0.774, respectively, for the first consensus guidelines; and 0.724, 0.779, and 0.801, respectively, for the second consensus guidelines, with balanced accuracies of 0.730 and 0.751, respectively. Multiple logistic regression analysis showed that main pancreatic duct dilatation >5 mm (hazard ratio [HR] 4.538; 95% confidence interval [CI], 2.449-8.408; P<0.001), mural nodules (HR 6.267; 95% CI, 3.271-12.009; P<0.001), and CA19-9 >37 U/ml (HR 4.032; 95% CI, 1.826-8.903; P=0.001) were independent predictors of malignancy of BD-IPMNs.

CONCLUSION: The second consensus guidelines showed better sensitivity, AUC and balanced accuracy than the first consensus guidelines in the diagnosis of BD-IPMN malignancy. However, size alone was limited in predicting malignancy. Additional tumor markers and imaging findings may be used as indicators for resection of BD-IPMN. The variability in clinical significance of each variable of the consensus guidelines indicates the need for a tailored approach in the management of patients with BD-IPMN.

S033 INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM OF THE PANCREAS, ONE MANIFESTATION OF A MORE SYSTEMIC DISEASE? Alexandra M Roch, MD, Carlo M Rosati, MD, Eugene P Ceppa, MD, Mohammad A Al-Haddad, MD, John M DeWitt, MD, C Max Schmidt, MD, PhD, MBA, FACS, 1 Department of Surgery, Indiana School of Medicine, Indianapolis, IN, USA; 2 Department of Medicine, Division of Gastroenterology, Indiana University Hospital, Indianapolis, IN, USA, Indianapolis, US

BACKGROUND: Several studies have demonstrated a high prevalence of extra pancreatic malignancies in patients with intraductal papillary mucinous neoplasm

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(IPMN) of the pancreas. Similarly, recent case reports have described an association between IPMN and autoimmune pancreatitis.

Hypothesis: We hypothesized that IPMN were associated with an increase rate of systemic disease (extra pancreatic malignancies and autoimmune disease).

METHODS: From 1996 to 2012, 841 patients with IPMN were seen at the pancreatic cyst clinic of a single academic institution. A retrospective analysis of a prospectively collected database was performed and supplemented with electronic medical charts review of clinical, radiological and (cyto) pathological parameters. Difference between observed and expected frequencies was assessed using Chi-square test. Fisher’s exact test compared IPMN type distribution - main pancreatic duct involved IPMN (MPD-involved IPMN) or branch-duct IPMN (BD-IPMN) - and rate of malignancy/invasiveness. P<0.05 was considered significant.

RESULTS: Among the 841 patients, 500 (59.5%) were followed whereas 341 (40.5%) underwent surgical resection for IPMN. Mean age was 68 years.

220 extra pancreatic malignancies were found in 185 patients (22%). The most common malignancies were colorectal adenocarcinoma (26/841, 3.1%), lung carcinoma (14/841, 1.7%) and renal cell carcinoma (14/841, 1.7%) with observed/expected frequencies ratio <0.0001 in those 3 cancers. However, the presence of extra pancreatic malignancy did not influence the subtype of IPMN (p=0.79), the rate of malignancy (p=0.81) or the rate of invasive carcinoma (p=0.89).

110 synchronous autoimmune diseases were found in 96 patients (11.4%). Systemic lupus erythematosus was found in 6/841 (0.7%), rheumatoid arthritis in 12/841 (1.4%) and inflammatory bowel disease in 15/841 (1.8%) with observed/expected frequencies ratio <0.0001, 0.014 and <0.0001, respectively. Patients associated autoimmune disease had a significantly higher rate of BD-IPMN (77.1% vs. 66.7%, p=0.048), resulting in lower rates of malignancy and invasive carcinoma (5.2% vs. 15.3% and 3.1% vs. 10.9%, p=0.005 and 0.017, respectively). However, when analyzed separately according to IPMN type, there was no influence of an associated autoimmune disease on malignancy/ invasiveness. Finally, in patients with autoimmune disease there was no impact of immunosuppressive treatment (steroids or immunosuppressant) on the subtype distribution (p=0.61), malignancy (p=0.66) or invasive carcinoma rates (p=0.9).

CONCLUSION: IPMN are associated with surprisingly high rates of extra pancreatic malignancies and autoimmune diseases (22% and 11.4%), suggesting that IPMN might be one manifestation of a more systemic disease.

S034 THE BIOLOGY OF SMALL IPMN CANCERS (< 20 MM INVASIVE COMPONENT): A MULTI-INSTITUTIONAL ANALYSIS Jordan M Winter, MD, Zhi V Fong, MD, Wei P Tan, MD, Wei Jiang, MD, PhD, Basturk Olca, MD, Mari Mino-Kenudson, MD, Harish Lavu, MD, Dana Haviland, David S Klimstra, MD, Murray F Brennan, MD, Keith D Lillemoe, MD, Charles J Yeo, MD, Carlos Fernandez-Del Castillo, MD, Peter J Allen, MD, Thomas Jefferson University, Massachusetts General Hospital, Memorial Sloan-Kettering Cancer Center, Philadelphia, US



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Recurrence risk of small invasive IPMN (p=0.4)No recurrence Recurrence

0 to 4.9 mm 29 (85%) 5 (15%)5 to 9.9 mm 11 (79%) 3 (21%)10 to 14.9 mm 4 (57%) 3 (43%)15 to 19.9 mm 7 (88%) 1 (12%)Total 51 (81%) 12 (19%)

BACKGROUND: Early invasive malignancy may be encountered in the background of intraductal papillary mucinous neoplasms (IPMN). The natural history of these invasive lesions is unknown.

METHODS: Pancreatic surgical databases from 3 high-volume centers (Thomas Jefferson University, Massachusetts General Hospital, and Memorial Sloan-Kettering) were queried for IPMN with invasive components <20 mm. Cases were reviewed by GI pathologists. A concensus between institutional pathologists was reached for difficult cases. Pathologic features were analyzed to identify predictors of recurrence.

RESULTS: A total of 63 small invasive IPMN (< 20 mm invasive component) were identified, comprising 35% of resected invasive IPMN (1993 to 2013). The median follow-up was 26 months (0.2 to 179). There were 16 deaths (25%), with a median estimated survival of 8 years. The overall recurrence rate was 19% (n=12) and the average time to recurrence was 15 months (4 to 132). Recurrence patterns were local in 33%, distant in 42%, and both in 25%. The majority of invasive foci were multifocal (73%) and involved the main duct (95%), with neither feature associated with recurrence. Papillary patterns included intestinal (51%), pancreatobiliary (17%), gastric (16%), oncocytic (10%), and mixed (6%), with comparable recurrence rates (18% to 50%, p=0.4). Cancer subtypes included tubular (52%), colloid (32%), oncocytic (11%), mixed (3%), and signet ring (2%), again with comparable recurrence rates (10 to 43%, p=0.4). Microscopic vessel invasion was identified in one patient (2%), perineural invasion in 19%, and microscopic lymphatic invasion in 15%. Regional lymph node metastasis was present in 16%, and correlated with lymphatic invasion (p<0.001). Unadjusted predictors of recurrence included lymph node metastasis (60% vs. 11%, p=0.001), lymphatic invasion (50% vs. 18%, p=0.04), and perineural invasion (42% vs. 14%, p=0.03). Dysplasia at the neck margin was observed in 19% of cases, but was not associated with recurrence (33% vs. 13%, p=0.1). The size of invasive foci was not associated with recurrence risk (p=0.4, table). Adjuvant treatment (16% of patients) was associated with a non-significant increase in recurrence risk (40% vs. 17%, p=0.1). In a multivariate model (dysplastic margin, perineural invasion, lymph node metastasis), lymph node metastasis was associated with recurrence (OR 11, p=0.005). Patients harboring small invasive IPMN without lymph node metastasis or perienural invasion still had a 9% recurrence risk.

CONCLUSION: The majority of small IPMN cancers are successfully treated with resection. However, recurrence risk is significant, and greatest in patients with lymph node metastases. Whether recurrences represent progression of residual

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disease or metachronous disease is unknown. Due to incomplete follow-up, these data likely underestimate the true recurrence rate.

S035 A NATIONAL PERSPECTIVE OF INVASIVE INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM (IPMN) Russell S Lewis, BS, Jeffrey A Drebin, MD, PhD, Douglas L Fraker, MD, Charles M Vollmer, MD, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, US

INTRODUCTION: Great understanding of IPMN has occurred in the last two decades, however questions remain which cannot be adequately answered by currently available institution-based literature. Specifically, 1) What are predictors of survival in these malignancies? 2) What is the impact of adjuvant therapy in this cohort? 3) How do outcomes compare to standard pancreatic ductal adenocarcinoma (PDAC)? A large scale assessment of invasive IPMN using a national dataset would provide greater clarity to these clinical dilemmas.

METHODS: Surgical patients from the National Cancer Database (NCDB) with histologically confirmed invasive IPMN were studied from 1998-2005 and compared to those with PDAC. Patients were excluded if they received preoperative systemic or radiation therapy, or if they died within 30 days of the operation. Survival was assessed using the log-rank test statistic and Cox regression.

RESULTS: 1739 patients underwent pancreatic resection for invasive IPMN (54% N0, 70% R0, median tumor size=3.5cm). 31% of patients were Stage 1, 33% Stage 2, 20% Stage 3, 11% Stage 4, and 5% were unclassified. For the overall cohort, median, 1-yr, and 5-yr survivals were 26.7m, 74%, and 32%. Adjuvant therapy was used in 45% of patients (24% in Stage 1 vs. 58% in Stages II-IV). The majority of treated patients received combined Chemo/XRT (70%). When assessed by Cox regression, improved survival for invasive IPMN was associated with receipt of adjuvant therapy (HR= 0.76; p<0.001), treatment at academic facilities, low grade tumors, N0 status, R0 resection, lower AJCC stage, and younger age. Furthermore, Cox models by stage revealed a survival advantage associated with adjuvant therapy in patients with Stage II-IV disease (HR 0.66; p<0.001), but not in Stage I (HR 1.21; p=0.223). IPMN had significantly better stage-adjusted survival than PDAC (table).

CONCLUSIONS: Invasive IPMN appears to be more indolent than standard PDAC, even after stage adjustment. Overall, adjuvant therapy improves survival for invasive IPMN, especially in higher-staged disease (by 34%). However, this benefit is not evident in early stage disease, negating the necessity of post-operative therapy in these situations.

AJCC Stage IPMN, suvival (mo.) PDAC, survival (mo.) P-value1 80.4 24.6 <0.0012 24.1 17.6 <0.0013 16.8 14.4 0.0104 10.1 9.8 0.318Overall 26.7 16.2 <0.001



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S036 CHARACTERIZATION OF PANCREATIC STROMAL CELLS ISOLATED FROM PANCREATITIS AND PANCREATIC ADENOCARCINOMA SURGICAL SPECIMENS Song Han, PhD, Daniel Delitto, MD, Jose G Trevino, MD, Kevin E Behrns, MD, Steven J Hughes, MD, Department of Surgery, University of Florida, Gainesville, US

INTRODUCTION: Accumulating evidence implicates the desmoplastic stromal compartment of the pancreatic cancer microenvironment as an integral factor in tumor development. However, the precise mechanisms of stromal contribution to cancer progression and the development of chemoresistance remain poorly characterized. We present a reproducible model capable of isolating pancreatic stromal cells from surgical specimens for further investigation into tumor-stromal interactions.

METHODS: Primary human pancreatic tissue was received fresh from surgical resections at the University of Florida’s high volume pancreatic surgery center. Pancreatitis, heavily implicated as a precancerous state, was included in a separate group from normal pancreas and pancreatic adenocarcinoma. Tissue fragments were minced and cultured in Dulbecco’s Modified Eagle Medium (DMEM) with 10% fetal bovine serum (FBS). Resulting stromal cells isolated in this manner were cultured and population doubling times were recorded. After 5-7 passages, cultured cells were further characterized with flow cytometry and immunohistochemical analysis. Specifically, markers of epithelial (ESA) or stromal (GFAP, α-SMA) differentiation as well as senescence (α-H2AX, Ki-67) were examined. Pancreatic stromal cells were then co-cultured with established pancreatic cancer cell lines (BxPC3, L3.6pl and PANC-1) and supernatants were assayed for differential cytokine secretion using Luminex analysis.

RESULTS: A total of 35 surgical specimens were investigated. Successful outgrowth of stromal cells was achieved in 3/5 (60%) normal pancreas samples, 5/6 (83%) pancreatitis samples and 23/24 (96%) pancreatic adenocarcinoma samples. Senescence occurred at 9.37+/- 0.38 (mean +/- SD) population doublings without significant variation between groups. Flow cytometry revealed α-SMA expression in over 95% and ESA expression in less than 5% of cultured stromal cells in all groups. These results were compared to a commercially available immortalized pancreatic fibroblast cell line, characterized by less than 1% α-SMA expressing cells and 58% ESA expressing cells. Co-culture of cancer-associated stroma with established pancreatic cancer cell lines revealed a 100-1,000-fold increase in SDF-1 expression compared with cancer cells cultured alone. This trend was observed across all established cancer cell lines co-cultured with three different stromal grafts.

CONCLUSION: Our model provides a reliable method for in vitro isolation of pancreatic stromal cells from human specimens in order to further characterize the microenvironment in pancreatitis and pancreatic cancer. Outgrowth of stromal cells in this manner demonstrates high levels of α-SMA expression and minimal ESA expression, indicative of pancreatic myofibroblastic differentiation. Additionally, co-culture of cancer-associated stroma obtained from our model

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with established cancer cell lines resulted in significantly elevated SDF-1 secretion, which is in agreement with current literature regarding paracrine signaling between cancer-associated stroma and pancreatic cancer cells.

S037 CURRENT INDICATIONS FOR SURGERY OF IPMN’S MAY OVERLOOK SOME PATIENTS WITH CANCER: RECOMMENDATIONS FOR CHANGE Andrew H Nguyen*, Paul Toste*, James J Farell#, Barbara M Clerkin*, V. Raman Muthusamy ,̂ Rabindra Watson ,̂ James S Tomlinson*, O. Joe Hines*, Howard A Reber*, Timothy R Donahue*, * Department of Surgery, David Geffen School of Medicine at UCLA, # Yale Center for Pancreatic Disease, Yale University School of Medicine, ^ UCLA Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, US

INTRODUCTION/BACKGROUND: Over the past decade, the management of intraductal papillary mucinous neoplasms (IPMN) has continued to evolve. Due to the high risk of cancer, almost all patients with main or mixed duct IPMN are recommended to undergo surgical resection. However, there continues to be debate in the management of patients with branch duct IPMN (BD-IPMN), which is associated with a lower risk of invasive malignancy. The revised Sendai Criteria of 2012 place less emphasis on the size of the lesion, and recommends that BD-IPMN ≥3 cm on noninvasive imaging (NIM) be interrogated by endoscopic ultrasound (EUS) for further “worrisome features.” Those lesions without a mural nodule/solid component or atypical cells on fine needle aspiration (FNA) should undergo observation rather than surgical resection. This change has generated significant concern amongst physicians treating pancreatic cystic lesions. Therefore, the aim of this study was to perform a retrospective review of BD-IPMN resected at a high volume pancreatic surgical center to determine: (i) the preoperative variables associated with malignancy and (ii) the optimal size cutoff on NIM to identify patients who should undergo EUS to identify those with advanced pathology.

METHODS: 66 patients with BD-IPMN between July 1996 to June 2012 at a high volume pancreatic surgical program at an academic medical center were identified in a prospectively maintained database of patients who underwent pancreatic resection. BD-IPMN were initially characterized by pre-operative CT/MRI and later confirmed by pathologic review. BD-IPMN was defined as a cystic dilation of the pancreatic duct, but not involving the main duct. Demographic, pathologic, and imaging data were extracted. Pathologic grade was dichotomized into (i) low (low or intermediate grade lesions) versus (ii) high (high grade, carcinoma in situ or invasive cancers). Fisher’s exact test, t-test, and receiver operator characteristic (ROC) analysis were performed.

RESULTS: The median cyst size on NIM was 2.7 cm (range: 0.6-9.6 cm), which correlated with final pathologic size (R2 = 0.819, p<0.001). Fifty-one (77%) low and 15 (23%) high grade BD-IPMN were identified. ROC analysis demonstrated that lesion size (on NIM) is a reasonable predictor of grade with an area under the curve of 0.691. Two-thirds of high grade BD-IPMN were <3 cm (n = 10). Compared with a cutoff of 3.0 cm, a NIM size cutoff of 2.0 cm: was associated with higher sensitivity (73.3% vs. 33.3%) and negative predictive value (83.3% vs 80%) for high



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grade IPMN. In fact, all smaller size cutoffs had higher NPVs than 3.0 cm. Mural nodules or atypical cells on FNA were identified in all cysts <2.0 and only 50% of those <3.0 cm.

DISCUSSION/CONCLUSIONS: Small cysts less than 3.0 cm can harbor high grade lesions or even invasive cancer. Our data suggests a need for further evaluation by EUS of smaller cysts. These results are opposite the trend of the revised 2012 Sendai Criteria towards greater observation and surveillance of larger cyst sizes.

S038 MAIN PANCREATIC DUCT SIZE AND RISK OF MALIGNANCY IN INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM Neda Rezaee, MD, Lindsey L Manos, PAC, Siva P Raman, MD, Elliot K Fishman, MD, Ralph H Hruban, MD, Timothy M Pawlik, MD, MPH, PhD, Matthew J Weiss, MD, Anne Marie Lennon, MD, PhD, Christopher L Wolfgang, MD, PhD, FACS, Department of Surgery, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins Medical Institutions, Baltimore, Maryland, Baltimore, US

BACKGROUND: Main pancreatic duct involvement by intraductal papillary mucinous neoplasm (IPMN) of the pancreas is associated with a high risk of invasive adenocarcinoma. The definition of what constitutes main duct or mixed type IPMN based on duct size is variable. Very few published work is available that documents risk of malignancy as a function of the size of the main pancreatic duct. The aim of this study was to identify an optimal duct size to contribute to main duct type IPMN.

METHODS: Data of patients with preoperative CT scan study who underwent surgical resection for an IPMN from 1996 to 2013 was analyzed. CT scans of the patients were reviewed by a radiologist where imaging was available. Main pancreatic duct (MPD) size was determined by the maximal cross-sectional diameter perpendicular to the long axis of the duct. IPMNs with low or intermediate grade of dysplasia were stratified as “low-risk”, and lesions with high-grade dysplasia or invasive carcinoma as “high-risk” disease.

RESULTS: A total of 420 consecutively resected IPMNs with adequate preoperative imaging data were identified. On final pathology 67 (16%) IPMNs were classified as low-grade dysplasia, 160 (38%) with intermediate grade dysplasia, 95 (23%) with high-grade dysplasia, and 98 (23%) with invasive carcinoma. MPD was < 5mm (small duct) in 224 (53%), 5-9 mm (intermediate duct) in 128 (30%), and >9 mm

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(large duct) in 68 (17%) patients. High risk IPMN was found in 26% small duct, in 63% intermediate, and 78% large duct IPMNs. Area under the receiver operating characteristics curve (AUR) of the MPD for predicting high risk IPMN was 75% (95% CI: 0.70- 0.80). The duct size of 5-mm was associated the optimal intersection of sensitivity (69%) and specificity (73%). The positive predictive value of the 5-mm duct threshold for high risk lesions was 68% and the negative predictive value was 74%. When the duct was dilated to ≥ 5mm, the incidence of high-risk IPMN wasnot different in lesions with diffuse (73%) or focal (59%) duct dilatation (p=0.06).

CONCLUSION: Preoperatively identified main pancreatic duct dilatation is an important factor in guiding the management of the IPMNs. Based on the increased risk of high-grade dysplasia and invasive carcinoma, surgical resection should be strongly considered when the MPD is diffusely or focally dilated to ≥ 5mm.

S039 DOES EUS IMPROVE OUTCOME IN SURVEILLANCE OF NON-RESECTED PRESUMED BRANCH-DUCT INTRADUCTAL PAPILLARY MUCINOUS NEOPLASMS? Anna C Evans, MD, Tarun Rustagi, MD, James J Farrell, MD, Yale-New Haven Hospital Internal Medicine Department; Yale Center for Pancreatic Disease, Interventional Endoscopy, Yale School of Medicine, New Haven, CT, New Haven, US

BACKGROUND: Current guidelines support surveillance with non-invasive imaging for presumed branch duct intraductal papillary mucinous neoplasms (BD-IPMN), not initially managed with surgery. There is little data regarding the optimal frequency, modality and long-term outcomes of both non-invasive (CT/MRI) and invasive (EUS) surveillance in these patients. We aim to perform a systematic review of all published studies to better define current surveillance strategies and outcomes in these patients.

METHODS: MEDLINE and Embase database searches were performed to identify studies with BD-IPMN patients that were initially managed non-surgically and



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surveyed for ≥ 3 months. Data regarding study design, number of patients, modality and frequency of surveillance, followup duration, change in cyst characteristics, development of pancreatic malignancy, and impact of surveillance on management was extracted.

RESULTS: Of 677 citations identified, 39 studies with 3745 BD-IPMN patients were included for analysis. Overall mean per-patient follow-up was 40.1±20.7 months. Morphologic progression of cystic lesions including new signs concerning for malignancy (increase in size, development of nodularity) was noted in 22.24% of patients (n=31 [79%] studies). 15.28% patients underwent surgical resection of cysts (n=37 [95%] studies). Pancreatic cancer developed in 141 (4.42%) patients (n=32 [82%] studies). Calculated risk of developing pancreatic cancer in BD-IPMN patients was 1.3% per year. 70 (4.36%) patients died during follow-up (1.38% per year; n=17 studies). Surveillance was done using CT (n=34 [87%] studies), MRI/MRCP (n=31 [79%] studies) and EUS (n=24 [62%] studies), with all three modalities of surveillance being used in 21 (54%) studies involving 55% of all BD-IPMN patients. 28 of 39 studies (81% of all BD-IPMN patients) reported change in management based on surveillance results. There was a statistically significant lower rate of surgical resection (p<0.00001) and overall mortality (p=0.0004) in patients undergoing surveillance which included EUS, compared with those who did not undergo EUS as part of their surveillance (Table 1).

CONCLUSIONS: Although this study has the limitations of a systematic review, it represents the most comprehensive study regarding long-term outcomes and surveillance techniques in BD-IPMNs. In addition to confirming the 1% yearly rate of cancer development in surveillance, this study strongly suggests that including EUS in surveillance of BD-IPMN may decrease mortality and reduce the need for surgery, and warrants further study.

Table 1. Outcomes for EUS surveillance in presumed BD-IPMN patients

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S040 RESECTED PANCREATIC ADENOCARCINOMAS WITH RECURRENCE LIMITED IN LUNG HAVE A SIGNIFICANTLY BETTER PROGNOSIS THAN THOSE WITH OTHER RECURRENCE PATTERNS Lei Zheng, MD, PhD, Tamna Wangjam, MD, Zhe Zhang, MS, Xiao Chong Zhou, MS, Laxmi Lyer, MD, Farzana Faisal, BS, Kevin C Soares, MD, Elliott Fishman, MD, Ralph H Hruban, MD, Joseph Herman, MD, Daniel Laheru, MD, Matthew Weiss, MD, Ana De Jesus-Acosta, MD, Christopher L Wolfgang, MD, PhD, Johns Hopkins University School of Medicine, Baltimore, US

INTRODUCTION/BACKGROUND: Majority of resected pancreatic adenocarcinoma (PC) recurs within 5 years of resection. However, the prognosis of different patterns of recurrence, particularly in the lung, has not been well studied.

METHODS: Between 1998 and 2007, 209 consecutive patients had surgical resection of PC and had postoperative follow-up primarily at the Johns Hopkins Hospital. A retrospective analysis of the 174 cases of recurrent PC out of the 209 patients was performed. Survival distributions among different patterns of recurrence were described using the Kaplan-Meier method and compared using Cox proportional hazards models.

RESULTS: With a median follow-up of 16 months (range 0.8-142.9), 174 of the 209 patients had recurrent diseases. Of those, 28 (13.4%) had metastatic recurrent diseases limited to lung only, 20 (9.6%) had recurrence in lung with one or more sites excluding liver, 73 (34.9%) had liver metastasis alone or with any other site except lung, 28 (13.4%) had local recurrence only, and 25 (12.0%) had peritoneal recurrence alone or together with local recurrence.

Patients with recurrence limited to lung had a 8.5 Mo median survival time from recurrence to death (RTD) and a 27.8 Mo median survival time from surgery to death (STD), which was significantly better than recurrence at any other site such as liver, peritoneum and local site in multivariate analyses after adjusting for age, tumor margin, tumor size, lymph nodes, and time from surgery to diagnosis of recurrence (for RTD, Liver vs. Lung: HR 1.90, p=0.022; Peritoneum vs. Lung: HR 6.32, p<0.0001; Local vs. Lung: HR 2.09, p=0.025). Interestingly, among all groups with different recurrence patterns, the time from surgery to the diagnosis of recurrence (STR) in patients who recurred in lung only (12.7 Mo) is also the longest. However, 75% of patients were found to have undetermined lung nodules in their surveillance CT scans prior to the diagnosis of recurrence in lung, suggesting they may have developed lung metastases long before the diagnosis. The median time from the surgery to the initial presentation of lung nodules is only 10.2 Mo, similar to the time of STR in liver (8.9 Mo), peritoneum (10.6 Mo) or local site (10.4 Mo). Nevertheless, whether there was a delay in the diagnosis of the lung nodules as the recurrence in lung did not have an impact on the survival (for RTD, HR=1.39, p=0.499).

DISCUSSION/CONCLUSIONS: The frequency of surgically resected PC with lung recurrence is much higher than was thought historically. PC with lung recurrence has a significantly better prognosis than recurrence in other sites although the diagnosis of lung recurrence was often delayed. Further studies are needed to investigate how different diagnostic and treatment modalities affect the survival of this unique subpopulation of PC patients.



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S041 THE INDOLENT NATURE OF PULMONARY METASTASES FROM PANCREATIC CANCER Stephanie Downs-Canner, MD, Mazen Zenati, MD, MPH, PhD, Brian A Boone, MD, Patrick R Varley, MD, Melissa E Hogg, MD, Amer H Zureikat, MD, Herbert J Zeh, MD, Kenneth K Lee, MD, University of Pittsburgh Medical Center, Pittsburgh, US

INTRODUCTION: Pulmonary metastases from pancreatic cancer are less common than intra-abdominal metastases and little is known about their natural history. Based on our observations, we hypothesize that among patients with lung metastases, those with pulmonary metastases first will have improved survival compared to those with intra-abdominal metastases as a first or synchronous site of disease.

METHODS: We performed a retrospective review of patients from 2001-2010 with a diagnosis of pancreatic cancer and pulmonary metastases. Demographic and clinicopathologic data were obtained from the electronic medical record and data was analyzed using Cox regression and the log rank test for survival analysis. The cohort was divided into four groups defined by first radiologic site of metastases: lung as the only site, lung as the first but not only site, abdomen as the first site and synchronous intra-abdominal and lung metastases.

RESULTS: 174 patients with pulmonary metastases from pancreatic cancer were identified. The average age was 66.9 (S.D. 10.7). 55.7% of patients were female. 44% of patients in the cohort had resection of their primary tumors prior to development of metastatic disease. There were no differences in age, race, gender, BMI, ASA, age adjusted Charlston Comorbidity Index (CCI) and history of alcohol or tobacco use based on the first site of metastases. Utilizing Kaplan-Meier survival analysis, we demonstrated significant differences in survival between all four groups, with patients developing lung metastases only or lung metastases first having improved survival compared to those with abdominal metastases first. Compared with patients who only developed lung metastases, patients with lung metastases first followed by intra-abdominal metastases had a hazard ratio of death of 1.42 (95% C.I. 0.89-2.25, p=0.140). Those with intra-abdominal metastases before lung metastases had a hazard ratio of death of 2.36 (95% C.I. 1.56-3.56, p<0.0001) and those with synchronous metastases had a hazard ratio of death of 3.78 compared to those with lung metastases only (95% C.I. 2.46-5.8, p<0.0001). These differences were independent of age, CCI, neoadjuvant chemotherapy, resection of the primary tumor and the T and N stage of primary tumors. There was also improved survival when patients with lung metastases as either the only or the first site of metastases were compared to those with intra-abdominal metastases first and synchronous metastases (p-value <0.0001). Again, this difference was independent of patient factors. Upon analysis of only those patients who underwent resection of their primary tumor, the difference in survival between groups remained statistically significant. Median survival among those who developed lung only or lung first recurrence was 37.5 months and 33.8 months respectively compared to 21 months for those with intra-abdominal recurrence or synchronous recurrence.

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CONCLUSION: In this large retrospective cohort of pancreatic cancer patients with lung metastases, those with lung metastases first had improved survival compared to those with intra-abdominal metastases first. These results suggest an indolent nature to pulmonary metastases. Further research is needed to determine how these results may impact clinical treatment decisions in patients with isolated pulmonary metastases.

S042 PANCREATIC STELLATE CELL SECRETED IL-6 MEDIATES STAT3 DEPENDENT CANCER CELL INVASION Jason A Castellanos, MD, M Ambrose, Y Beesetty, N Nagathihalli, PhD, N B Merchant, MD, Vanderbilt University Medical Center, Nashville, US

INTRODUCTION: Pancreatic cancer is the fourth most common cause of cancer-related death in the United States. Pancreatic ductal adenocarcinoma (PDAC) is an inflammatory disease and includes several stromal elements such as immune cells, fibroblasts, and stellate cells. Pancreatic stellate cells (PSCs) are myofibroblast-like cells responsible for the dense tumor stroma, which is a hallmark of PDAC. The role of tumor-associated stroma in PDAC is not well understood. The purpose of this study was to determine if factors produced by PSCs could effect signaling and tumorigenicity in cancer cells. We hypothesized Interleukin (IL)-6 secreted from PSCs activates STAT3 signaling and enhance tumor invasion in PDAC cells.

METHODS: Total and activated STAT3 expression was determined in human and mouse PSCs, human PDAC cell lines, a human pancreatic ductal epithelial (HPDE) cell line and cell lines generated from Pdx-cre/LSL-KrasG12D and Pdx-cre/LSL-KrasG12D/LSL-p53R273H mice. A panel of cytokines and chemokines were analyzed in PSC culture supernatants. IL-6 concentrations were determined in PSC supernatants by ELISA. Lysates from cells treated with PSC-conditioned medium (PSC-CM) were assayed for protein expression for STAT3, pSTAT3, STAT5, pSTAT5, STAT1 and pSTAT1 by immunoblot. Colony formation and cell invasion assays were performed with and without neutralizing IL-6 antibody, STAT3 inhibitor (AZD1480) and in STAT3 shRNA Panc1 cells.

RESULTS: STAT3 activation is necessary for malignant phenotype and affects survival in PDAC. PSCs produced cytokines that have a documented role in promoting tumor progression. Supernatants from PSCs contained significantly higher concentrations of IL-6 compared with other cytokines. Exposure to PSC-CM activated STAT3 signaling in Panc1 and MiaPaca PDAC cells and significantly enhanced both cell invasion and colony formation. Neutralization with IL-6 antibody in the PSC-CM prevented phosphorylation of STAT3 and abrogated the ability of PSCs to induce cell invasion and stimulate colony formation. Pharmacologic inhibition of STAT3 (AZD 1480) or siRNA knockdown of STAT3 in Panc1 cells similarly inhibited both cell invasion and colony formation associated with exposure to PSC-CM.

CONCLUSIONS: PSCs release IL-6, which promotes STAT3-dependent signaling and tumorigenecity in PDAC. These findings demonstrate a novel role of PSCs in supporting an inflammatory tumor microenvironment and extend the evidence of crosstalk between the tumor stroma and epithelium. Furthermore, these results show that STAT3 may represent a therapeutic target in PDAC.



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S043 NEUTROPHIL EXTRACELLULAR TRAPS (NETS) ARE UPREGULATED IN PANCREATIC CANCER AS A RESULT OF AUTOPHAGY AND CONTRIBUTE TO HYPERCOAGULABILITY Brian A Boone, MD, Nicole Schapiro, MS, Lidiya Orlichenko, PhD, Matthew D Neal, MD, Jarrod Ellis, Michael T Lotze, MD, Herbert J Zeh, MD, University of Pittsburgh, Pittsburgh, US

INTRODUCTION: Neutrophil extracellular traps (NETs) occur when activated neutrophils release their intracellular contents containing DNA, histones and granule constituents to trap and kill bacteria. While traditionally associated with sepsis, NETs have also been demonstrated in sterile inflammation and have been linked to thrombosis. Recently, the process of autophagy has been implicated in NET formation. We have previously reported that pancreatic ductal adenocarcinoma (PDA) is associated with increased autophagy in the tumor microenvironment and systemically. Here were explored NETs and autophagy in models of murine and human PDA as well as their potential role in hypercoagulability of cancer.

METHODS: Neutrophils were isolated from both an orthotopic and a genetically engineered murine model of PDA (Pdx-1-Cre/LSL-KRasG12D, KC) utilizing density gradient centrifugation. NETs were induced with platelet activating factor (PAF,0-40µM) and visualized by Hoechst staining to identify both nuclear and extracellular DNA. Levels of free DNA were measured as a surrogate marker of NET formation in PDA in murine and patient serum. Animals were treated with the autophagy inhibitor chloroquine (CQ, 100 mg/kg/day PO) as well as DNase (100U IP x 4 doses). Thromboelastograms (TEG) were performed on blood from tumor bearing and control animals.

RESULTS: Neutrophils from tumor bearing animals (KC and orthotopic) were more prone to NET formation following PAF stimulation (Figure). Pre-treatment of harvested neutrophils with CQ prior to PAF stimulation reversed the tumor bearing effect. Treatment of tumor bearing animals with CQ also reversed the propensity to form NETs. Serum DNA was elevated in the orthotopic animals compared with sham controls (80 vs. 38 ng/mL, p<0.05) and in the KC animals compared with wild type (WT) (56 vs. 42 ng/mL, p<0.05). Treatment with CQ decreased serum DNA in both tumor bearing models. 80% of patients had a decrease in serum DNA following treatment with gemcitabine + CQ. Treatment with DNase also decreased serum DNA in the orthotopic animals. Orthotopic tumor bearing animals were hypercoagulable on TEG compared to sham controls. These effects were partially reversed with chloroquine or with DNase treatment.

CONCLUSION: Mice from both orthotopic and genetically engineered models of pancreatic cancer demonstrate increased propensity for NET formation associated increased free serum DNA . In vitro and in vivo treatment with the autophagy inhibitor chloroquine reversed this process. This suggests that pancreatic cancer results in an increase in NET formation through an autophagy mediated process. Additionally, NETs in pancreatic cancer may contribute to hypercoagulability.

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Figure 1

S044 ISOLATION AND CHARACTERIZATION OF DCLK1+ TUMOR CELLS OF PANCREATIC ADENOCARCINOMA PATIENTS Jeremy L Irvan, MD, Dongfeng Qu, PhD, Alexander Raines, MD, Parthasarathy Chandrakesan, Nathaniel Weygant, Randal May, Shubham Pant, MD, Courtney W Houchen, MD, Russell G Postier, MD, University of Oklahoma, Oklahoma City, US

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) has the worst prognosis of any major malignancy with less than a 6% 5-year survival rate. It is one of the leading causes of cancer-related death in the developed world and is the fourth leading cause of cancer death in the United States. Patients with PDAC are often diagnosed at late stages with extensive local tumor invasion and early metastasis, presenting a major obstacle to all forms of therapy. Cells with cancer stem cell (CSC) properties were identified in PDAC. CSCs are often resistant to chemotherapy and radiation therapy, this may explain why current treatments do not cure PDAC or prevent recurrences. It is suggested that stem cells may be the root of PDAC. Targeting CSCs is a very promising therapeutic approach for PDAC. Doublecortin-like kinase 1 (DCLK1), a microtubule-associated kinase, is a putative pancreatic stem cell marker and is upregulated in pancreatic cancer, colorectal cancer, and many other solid tumor cancers. It marks tumor stem cells in mouse models of intestinal neoplasia. The aim of this study is to evaluate the stemness, pluripotency, and clonogenicity of DCLK1+ tumor cells isolated from PDAC patients.

METHODS: Tumor tissues were obtained after resection from three stage IIA and IIB PDAC patients. Tumor tissues were digested with collagenase IV and single cell suspensions were filtered and cultured. Cultured PDAC tumor cells were passed and expanded for eight passages. DCLK1+ tumor cells were isolated using anti-DCLK1 antibody and FACS-based cell sorting. Gene expressing levels in both DCLK1+ and DCLK1- cells were analyzed by real-time RT-PCR. The proliferative, invasive, and clonogenic activities of DCLK1+ and DCLK1- cells were compared using MTT assay, migration assay in 24-well transwell coated with Matrigel, and clonogenicity assay in soft agar.



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RESULTS: We successfully cultured the primary tumor cells isolated from PDAC tumor tissues, and passed the cells more than ten generations. We found that the expressing levels of pluripotency factors, SOX2, NANOG, OCT4, and LIN28, were 2 fold higher in the isolated DCLK1+ cells compared to that in DCLK1- cells. The expression levels of pancreatic cancer related oncogenes, KRAS, NOTCH, and REG4, were significantly increased in the DCLK1+ cells compared to that in the DCLK1- cells. The expression levels of epithelial mesenchymal transition (EMT) related genes, ZEB1, ZEB2, SNAIL, SLUG, and TWIST, were also significantly increased in the DCLK1+ cells compared to that in the DCLK1- cells. Both isolated DCLK1+ and DCLK1- cells were subjected to MTT assay, the isolated DCLK1+ cells exhibited increased proliferation activity compared to that in the DCLK1- cells. Furthermore, DCLK1+ cells have increased migration activity and clonogenic activity compared to DCLK1- cells.

CONCLUSION: These results demonstrated that DCLK1+ cells have increased pluripotency, stemness, migrative, and clonogenic activities, suggesting that DCLK1 marks pancreatic tumor stem cells. These results also suggest that targeting DCLK1 may have therapeutic potential in PDAC.

S045 SEQUENCE ALTERATIONS IN THE WEE1 NON-CODING REGION IS A FACILITATOR AND MARKER FOR PANCREATIC TUMORIGENESIS Shruti Lal, PhD, Joseph A Cozzitorto, Fernando F Blanco, PhD, Janae Romeo, Charles J Yeo, MD, Jonathan R Brody, PhD, Jordan M Winter, MD, Thomas Jefferson University, Philadelphia, US

INTRODUCTION: We discovered an abnormal sequence motif in a 56 bp non-coding region of the mitotic kinase inhibitor WEE1 in pancreatic adenocarcinoma, which contains the binding site of an RNA binding protein, HuR (important for cancer cell survival). WEE1 promotes DNA repair by triggering a mitotic checkpoint in the setting of DNA damage. We hypothesized that a germline sequence alteration (INDEL, insertion/deletion of bases) in WEE1 impairs HuR stabilization of the WEE1 transcript and abrogates this critical checkpoint in cells, thereby enhancing proliferation. Paradoxically, this phenotype could render cells susceptible to DNA damaging agents.

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EXPERIMENTAL METHODS: The 56 bp HuR binding site on the WEE1 transcript was sequenced in 21 cancer cell lines, 30 familial pancreatic cancers, and 68 patients with normal pancreata. Functional assays were performed in cell lines with wild type and abnormal WEE1 sequence after treatment with mitomycin C (MMC).

RESULTS: An INDEL was identified in the poly-T track of the 56 bp region (ATGTACCTGTGTGTCCATCTTATATTTCTTTTTTTTTTAATTGTGAATTAGAC), which has 10 T’s in the wild type sequence. In the control group, 51 patients had two wild type alleles, and 17 were heterozygous for a TT insertion (12 T’s), establishing an abnormal allelic frequency of 12.5%. In 21 cancer cell lines, 10 were homozygous for the wild type sequence, and 11 exhibited a TT insertion. In 5 of these cell lines, the second allele exhibited a separate abnormality (11 T’s). In total, the abnormal allelic frequency was three-fold increased at 38%. In 30 familial pancreatic cancers, 12 were homozygous for the wild type sequence and 18 had the TT insertion (abnormal allelic frequency of 30%, p<0.0003 vs. controls). MMC (i.e., DNA damage) treatment of pancreatic cancer cell lines results in HuR movement from the nucleus to the cytoplasm with its bound mRNA (e.g., the WEE1 transcript). MMC induced WEE1 protein expression by Western blot in cell lines with wild type sequence, but not in cell lines containing INDELs in both alleles. Reporter constructs with luciferase in front of the HuR-WEE1 binding site (both wild type and abnormal sequence motifs) were generated. Upon treatment with MMC, reporter activity was reduced with plasmids containing the TT insertion (Figure). Interestingly, biallelic abnormal binding site sequences (while observed in 5/21 cancer cell lines) were never identified in the germline of any patients (n=98, expected in 5% of individuals), suggesting that the abnormal HuR binding site sequence is functionally important and embryonic lethal.

CONCLUSIONS: The incidence of a TT insertion in the HuR binding site on WEE1 is increased in familial pancreatic cancer and results in decreased WEE1 expression upon DNA damage. These findings may have important implications for 1) genetic screening, 2) predicting chemo-responsiveness, 3) and the development of novel therapies.

S046 CHEMOTHERAPY RESISTANT PANCREATIC CANCER TUMOR-ASSOCIATED FIBROBLASTS ARE PROTUMORIGENIC Paul A Toste, MD, Andrew H Nguyen, MD, Brian E Kadera, MD, Mindy Duong, Nanping Wu, PhD, Luyi Li, MS, Timothy R Donahue, MD, Department of Surgery, University of California, Los Angeles, Los Angeles, US

INTRODUCTION: As a result of late diagnosis and frequent resistance to cytotoxic chemotherapy, pancreatic ductal adenocarcinoma (PDAC) has a notoriously poor prognosis. An important component of chemoresistance in PDAC is the dense tumor-associated stroma (TAS) characteristic of the disease. PDAC tumor-associated fibroblasts (TAFs), the predominant cell type of the TAS, enhance tumor growth, invasion, metastasis, and chemoresistance. However, the impact of chemotherapy on TAF biology has not yet been reported.

METHODS: Immortalized human TAFs were grown in either standard media or media containing IC50 doses of gemcitabine for 4 weeks to generate chemotherapy-naïve and chemotherapy-resistant lines. Gene expression



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microarray analysis was performed to compare naïve and chemoresistant TAFs. Expression of selected targets was confirmed by qRT-PCR and/or antibody-based cytokine array. IL-8 expression was quantified by ELISA. Conditioned media (CM) was produced from both naïve and resistant TAFs. MTT assay was used to assess tumor cell (TC) viability in naïve versus resistant CM. TC migration and invasion as well as endothelial cell migration were assessed using modified Boyden chambers with naïve or resistant CM. For in vivo studies, TCs were subcutaneously co-implanted with naïve or resistant TAFs in immunodeficient mice.

RESULTS: Microarray analysis demonstrated that TAFs undergo a large number of molecular changes in response to cytotoxic chemotherapy. Molecules involved in important TAF functions such as stellate cell activation, cellular movement, extracellular matrix production and remodeling, and cytokine signaling were altered. Of note, the expression of multiple inflammatory molecules was increased. Cytokine array and qRT-PCR confirmed elevated levels of multiple inflammatory cytokines (IL-6, IL-8, CXCL-1, CXCL-6) in chemoresistant TAF conditioned media. Furthermore, ELISA demonstrated that IL-8 concentration was 6-fold higher in chemoresistant TAF CM compared to naïve TAF CM. TCs (Miapaca-2 and Panc1) demonstrated increased viability when grown in the presence of resistant as compared to naïve TAF CM (p<0.001). TCs also showed increased migration (Miapaca-2, p<0.001 and Panc1, p=0.002) and invasion (Panc-1, p<0.001) in the presence of resistant CM. Resistant TAF CM was also pro-angiogenic, as evidenced by increased endothelial cell migration (p=0.01). In vivo, TCs (Miapaca-2) implanted along with chemoresistant TAFs grew larger tumors compared to those implanted with naïve TAFs (p=0.004).

CONCLUSION: After treatment with cytotoxic chemotherapy, TAFs manifest multiple molecular changes including a pro-inflammatory gene expression signature. Chemoresistant TAFs support tumorigenesis and angiogenesis in vitro and in vivo via paracrine signaling. While further studies are needed to evaluate regulation and mediators of the TAF response to chemotherapy, it represents a potential therapeutic target to improve efficacy of current treatments in PDAC.

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S047 PTK6 INCREASES APOPTOSIS WITH GEMCITABINE TREATMENT IN PANCREATIC CANCER CELLS BY ENHANCING DNA DAMAGE Hiroaki Ono, MD, PhD, Marc D Basson, MD, PhD, Hiromichi Ito, MD, Michigan State University, East Lansing, US

BACKGROUND: Protein Tyrosine Kinase 6 (PTK6) is a non-receptor type tyrosine kinase known to be aberrantly expressed in various cancers including pancreatic cancer. The role of PTK6 in cancer chemo-resistance remains unknown. We tested our hypothesis that PTK6 regulates gemcitabine (GEM) resistance in pancreatic cancer, and explored its mechanism.

METHODS: We studied 2 human pancreatic cancer cell lines, Panc1 and MIAPaCa2. For some studies, GEM resistant clones of Panc1 and MIAPaCa2 were isolated by culture with GEM for 2 months. Cell survival was measured by WST-8 assay. GEM-induced apoptosis and DNA damage were evaluated by Western blotting. The effect of PTK6 overexpression on the efficacy of GEM therapy for pancreatic cancer in vivo was assayed using a xenograft mouse model.

RESULTS: Endogenous PTK6 expression was increased at 24-48 hours with GEM treatment in Panc1 and MIAPaCa2 cell lines. PTK6 gene-silencing increased cell survival after GEM treatment and decreased cleaved Caspase3 and PARP, indicating decreased apoptosis, while PTK6 overexpression decreased cell survival and increased apoptosis. Basal PTK6 expression was significantly reduced in the GEM resistant clones compared with the parental lines (0.29 fold decrease in MIAPaCa2 and 0.60 fold decrease in Panc1, respectively, p<0.05). Restoration of PTK6 expression using an over-expression vector made the resistant MIAPaCa2 clone cells sensitive to GEM (0.77 fold decreased survival compared to the resistant clone, p<0.05). To explore the mechanism in which PTK6 regulates the cytotoxic effect of GEM on pancreatic cancers, we tested the effect of altered PTK6 expression on DNA damage induced by GEM. GEM-induced H2AX phosphorylation (γ-H2AX), which is a specific marker for DNA double-strand breaks, was significantly reduced by PTK6 gene-silencing, while GEM-induced γ-H2AX was increased by PTK6 overexpression. Furthermore, PTK6 gene silencing also inhibited the GEM-induced activation of ataxia-telangiectasia mutated (ATM) protein kinase, a central initiator of key signal responses to DNA damages in both cell lines. Conversely, ATM kinase activation was enhanced by PTK6 overexpression (Figure). In the mouse xenograft model, subcutaneous tumors with PTK6-overexpressing MIAPaCa2 showed significant growth reduction compared with tumors with control MIAPaCa2 after 5 weeks treatment with GEM (150 mg/kg IP, twice a week) (606 mm3 vs 252 mm3 in size, 609 mg vs 128 mg in weight, p<0.01, respectively) .

CONCLUSION: PTK6 is endogenously activated by GEM treatment in pancreatic cancers, and forced-overexpression of PTK6 increases the efficacy of GEM on pancreatic cancer with enhancing DNA damage. Further study to elucidate the mechanism by which PTK6 regulates GEM-induced DNA damage may identify therapeutic targets to improve the outcomes of patients with pancreatic cancer.



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S048 THE VALUE OF DRAINS AS A FISTULA MITIGATION STRATEGY FOR PANCREATODUODENECTOMY: SOMETHING FOR EVERYONE? RESULTS OF A RANDOMIZED PROSPECTIVE MULTI-INSTITUTIONAL STUDY Matthew T McMillan, BA, William E Fisher, MD, Jeffrey Drebin, MD, PhD, Stephen Behrman, MD, Mark Bloomston, MD, Kimberly M Brown, MD, Steven J Hughes, MD, Katherine A Morgan, MD, Vic Velanovich, MD, Jordan Winter, MD, Nicholas J Zyromski, MD, Charles M Vollmer, MD, University of Pennsylvania School of Medicine, Baylor College of Medicine, Philadelphia, US

INTRODUCTION: A recent randomized controlled trial investigating intraperitoneal drain use during pancreatoduodenectomy (PD) had a primary goal of assessing overall morbidity. It was terminated early with findings that routine elimination of drains in PD increases mortality and the severity and frequency of overall complications. Here, we provide a subset analysis of drain value in reference to clinically-relevant postoperative pancreatic fistula (CR-POPF), with emphasis on risk-adjusted outcomes.

METHODS: Nine institutions performed 137 PDs, with patients randomized to intraperitoneal drainage (D; n=68) or no drainage (ND; n=69). CR-POPFs were categorized, at POD 60, as ISGPF Grade B or C. The Fistula Risk Score (FRS), a 10-point scale derived from four validated risk factors for CR-POPF (soft gland, small duct, high-risk pathology, increased blood loss), facilitated risk adjustment between groups. FRS risk zones include: Negligible (FRS 0), Low (FRS 1-2), Moderate (FRS 3-6) & High (FRS 7-10).

RESULTS: There was no difference in overall fistula risk between the two groups as judged by mean FRS (D=3.51 vs. ND=3.57; p=0.897), rates of each of the aforementioned individual risk factors, or stent use. When used, drains were typically removed POD 7. Overall, CR-POPF rates were higher in the no drain group compared to the drain group (20.3% vs. 13.2%; OR: 1.67; p=0.269), as were rates of the severe Grade C POPFs (8.7% vs. 2.9%; OR: 3.14; p=0.274). The use of drains in the presence of known individual FRS factors was associated with lower CR-POPF rates, particularly for soft glands (11.8% vs. 34.3%; OR: 0.26; p=0.027). For each cohort, CR-POPF occurrence was assessed across the various FRS risk zones. CR-POPF never occurred in the 10 patients with negligible risk. In patients with Low risk, the rate of CR-POPF was actually higher when drains were utilized (19.0% vs. 4.8%; OR: 4.71; p=0.343). Conversely, there were significantly fewer CR-POPFs (12.2% vs. 29.5%; p=0.050) when drains were used in Moderate and High risk scenarios (Figure). The benefit of drains in these particular patients is detailed in Table 1. Lastly, patients who suffered CR-POPFs experienced shorter duration of stay (15.2 d vs. 34.7 d, p=0.010) and reduced 90-d mortality (11.1% vs. 42.9%; OR: 0.17; p=0.176) when a drain was used.

CONCLUSION: Controversy exists over the efficacy of drains as a fistula mitigation strategy in cases of PD. The results of this analysis suggest that drains diminish the rate and severity of CR-POPF in patients with Moderate and High fistula risk, but they might be avoided in the roughly one-third of patients

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with Negligible or Low risk. The premature discontinuation of this study, due to obvious deleterious outcomes in the absence of drains, limits its statistical power; yet, the randomization process and risk adjustment with the FRS ensures absence of bias.

S049 A RANDOMIZED PROSPECTIVE MULTICENTER TRIAL OF PANCREATICODUODENECTOMY WITH AND WITHOUT ROUTINE INTRAPERITONEAL DRAINAGE George Van Buren, II, MD, Mark Bloomston, MD, Steven J Hughes, MD, Jordan Winter, MD, Stephen W Behrman, MD, Nicholas J Zyromski, MD, Charles Vollmer, MD, Vic Velanovich, MD, Taylor Riall, MD, Peter Muscarella, MD, Jose Trevino, MD, Attila Nakeeb, MD, Max Schmidt, MD, Kevin Behrns, MD, Christopher Ellison, MD, Omar Barakat, MD, Kyle Perry, MD, Jeffrey Drebin, MD, Michael House, MD, Sherif Abdel-Misih, MD, Eric J Silberfein, MD, Steven Goldin, MD, Kimberly Brown, MD, Somala Mohammed, MD, Sally E Hodges, BS, Amy McElhany, MPH, Mehdi Issazadeh, BS, Eunji Jo, MS, Qianxing Mo, PhD, William E Fisher, MD, 1Baylor College of Medicine, The Elkins Pancreas Center, Michael E. DeBakey Department of Surgery, and Dan L. Duncan Cancer Center, Houston, TX, Houston, US

OBJECTIVE: To test by randomized prospective multicenter trial the hypothesis that pancreaticoduodenectomy (PD) without the use of routine intraperitoneal drainage does not increase the frequency or severity of complications.

BACKGROUND: Some surgeons have abandoned the routine use of drains placed at the time of pancreas resection.



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METHODS: One hundred-thirty seven patients were randomized to PD with (n=68, drain group) and without (n=69, no-drain group) the use of routine intraperitoneal drainage and the safety of this approach and spectrum of complications between the two groups were compared.

RESULTS: There were no differences between drain and no-drain cohorts in demographics, comorbidities, pathology, pancreatic duct size, pancreas texture, baseline quality of life, or operative technique.

Pancreaticoduodenectomy without routine intraperitoneal drainage was associated with an increase in the number of complications per patient (1(0-2) vs. 2(1-4), p=.029); an increase in the number of patients who had at least one ≥ grade 2 complication (35 (52%) vs. 47 (68%), p=0.047); and a higher average complication severity (2 (0-2) vs. 2(1-3), p=0.027). Pancreaticoduodenectomy without routine intraperitoneal drainage was associated with a higher incidence of gastroparesis, intra-abdominal fluid collection, intra-abdominal abscess (10% vs 25%, p= 0.027), severe (≥ grade 2) diarrhea, need for a postoperative percutaneous drain, and a prolonged length of stay.

The study was stopped early by the Data Safety Monitoring Board due to a four-fold increase in mortality from 3% to 12%mortality in the patients undergoing PD without routine intraperitoneal drainage, many of whom had pancreatic fistulas.

CONCLUSION: This randomized prospective multicenter trial provides level one data suggesting that elimination of intraperitoneal drainage in all cases of PD increases the frequency and severity of complications and likely increases mortality.

S050 RISK-ADJUSTED OUTCOMES OF CLINICALLY-RELEVANT POSTOPERATIVE FISTULA FOLLOWING PANCREATODUODENECTOMY: A MODEL FOR PERFORMANCE EVALUATION Charles M Vollmer, MD, Matthew T McMillan, BA, Sameer Soi, MS, Benjamin C Miller, BA, Pancreas Fistula Study Group, University of Pennsylvania School of Medicine, Philadelphia, US

INTRODUCTION: Accurate assessment of surgeon and institutional performance requires: 1) establishment of a standard for comparison; 2) the ability to adjust for variability in patient risk and characteristics of surgeon and institution. We sought to evaluate surgical performance in pancreatoduodenectomy using clinically-relevant postoperative fistula (CR-POPF) occurrence as a quality indicator.

METHODS: This multinational, retrospective study of 4,187 pancreatoduodenectomies involved 55 surgeons at 15 institutions. Risk was assessed using the previously validated Fistula Risk Score (FRS) and fistulas were stratified by International Study Group criteria. CR-POPF variability was evaluated and hierarchical regression analysis assessed individual surgeon and institutional performance.

RESULTS: There was variability in both CR-POPF risk and occurrence (Table). Risk alone did not explain all observed outcomes; surgeon-specific effects (fistula mitigation choices) and institutional volume were important in accounting for discrepancies. The model identified variables that were associated with lesser (Stents – Odds Ratio[OR]=0.69; Drains OR=0.69) or greater (Octreotide OR=2.28;

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Pancreatogastrostomy OR=1.91) CR-POPF occurrence. When controlling for risk, performance outliers were identified, at both the surgeon and institutional levels (Figure).

CONCLUSIONS: This largest analysis of pancreatic fistulas following pancreatoduodenectomy demonstrates considerable variability in risk and occurrence of CR-POPF among surgeons and institutions. Beyond inherent patient risk factors, surgical decision-making influences fistula outcomes.

S051 HIGH PERFORMING WHIPPLE PATIENTS: FACTORS ASSOCIATED WITH SHORT LENGTH OF STAY AFTER OPEN PANCREATICODUODENECTOMY Grace C Lee, BS, Zhi Ven Fong, MD, Cristina R Ferrone, MD, Sarah P Thayer, MD, PhD, Andrew L Warshaw, MD, Keith D Lillemoe, MD, Carlos Fernandez-del Castillo, MD, Department of Surgery, Massachusetts General Hospital, Boston, MA, United States, Boston, US

INTRODUCTION: In this cost-conscious era of health care reform, much attention has been focused on minimizing length of hospital stay (LOS) and readmission



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rates after surgical procedures. Despite the decreasing morbidity and mortality of pancreaticoduodenectomy (PD), it continues to be associated with prolonged LOS. As preliminary data of minimally invasive PD emerges, we sought to determine the average LOS after open PD at a high-volume tertiary care hospital in an attempt to set a standard to which minimally invasive PD can be compared. We also determined the factors that could predict “high performance” after PD.

METHODS: The demographic, perioperative, and readmission data of 634 consecutive patients who underwent open PD between January 2007 and December 2012 at the Massachusetts General Hospital were reviewed. “High performers” were defined as patients with a LOS ≤5 days.

RESULTS: The median LOS was 7 days (interquartile range 6-10 days). A total of 61 patients (9.6%) had a LOS ≤5 days and were deemed “high performing”. Postoperative delayed gastric emptying, ICU admission, and discharge to a rehabilitation facility each perfectly predicted LOS >5 days. In multivariate logistic regression analysis, neoadjuvant therapy (26.2 vs 15.9%, OR 3.31, p=0.003), epidural success (92.9 vs 85.1%, OR 3.73, p=0.030), epidural duration ≤3 days (40.4 vs 19.5%, OR 2.90, p=0.002), surgery on Thursday or Friday (59.3 vs 46.1%, OR 3.10, p=0.001), and discharge on Monday through Wednesday (80.3 vs 50.7%, OR 6.54, p<0.001) were independently associated with LOS ≤5 days. Age ≤70 years, male gender, Charlson comorbidity index <5, and high surgeon volume were predictive of “high performance” on univariate analysis, but were not significant in the multivariate model. When comparing “high performing” patients to those with LOS>5 days, readmission rate (16.4% vs 22.2%, p=0.298) and time to readmission (5.5 vs 12 days, p=0.661) were not different. Body mass index, diabetes, prior abdominal surgery, prior ERCP, vessel resection, and tumor pathology also did not correlate with LOS.

CONCLUSION: In our contemporary experience of patients undergoing pancreaticoduodenectomy, median LOS after open PD was 7 days, with a 9.6% rate of “high performers”. LOS ≤5 days was associated with neoadjuvant therapy, epidural success, and undergoing surgery at the end of the week. “High performing” patients experienced no difference in readmission rates as a result of their early discharges. Minimally invasive PD should be compared to this high standard for LOS, among other quality metrics, to justify its increased cost and operative duration.

S052 THE ASSOCIATION BETWEEN PANCREATIC FISTULA GRADE C AND SURVIVAL AFTER PANCREATIC RESECTION FOR PANCREATIC CANCER Manabu Kawai, MD, PhD, Masaji Tani, MD, PhD, Seiko Hirono, MD, PhD, Ken-ichi Okada, MD, PhD, Fuyuhiko Motoi, MD, PhD, Michiaki Unno, MD, PhD, Masayuki Sho, MD, PhD, Yoshiyuki Nakajima, MD, PhD, Kenichiro Uemura, MD, PhD, Sohei Satoi, MD, PhD, A-Hon Kwon, MD, PhD, Ippei Matsumoto, MD, PhD, Tadahiro Goto, MD, PhD, Goro Honda, MD, PhD, Masanao Kurata, MD, PhD, Yoshiaki Murakami, MD, PhD, Hiroki Yamaue, MD, PhD, Multicenter Study Group of Pancreatobiliary Surgery (MSG-PBS), Wakayama, JP

BACKGROUND: Several studies demonstrated that postoperative complications after pancreatic resection for pancreatic cancer adversely affect survival outcome. Pancreatic fistula grade C is one of the most serious complications after pancreatic

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resection. However, it remains unclear whether pancreatic fistula grade C affects long-term outcome after resection for pancreatic cancer.

AIMS: The aim of this study is to elucidate the adverse effect of pancreatic fistula grade C on recurrence and survival after resection for pancreatic cancer by a survey of high volume center of pancreatic resection in Japan.

METHODS: Medical records were reviewed in 1,015 patients with pancreatic cancer who underwent pancreatic resection between 2001 and 2010 at 7 high-volume surgical institutions in Japan. Pancreatic fistula was defined based on the International Study Group on Pancreatic Fistula (ISGPF) guideline.

RESULTS: Overall morbidity following pancreatic resection was 42.6%, and 30-day mortality was 0.3%. Pancreatic fistula occurred in 22.9% (232 of enrolled 1,015 patients) ; grade A 9.4%, grade B 10.7%, grade C 2.8%. Concerning with disease-free survival, patients with pancreatic fistula grade C had a significantly shorter time to recurrence than those without it (5.8 vs. 12.6 months, p=0.019). Concerning with overall survival, patients with pancreatic fistula grade C had a significantly poorer survival than those without it (8.1 vs. 22.3 months; median survival, 14.3 vs. 32.6% months; 3-year survival, p<0.0001). Pancreatic fistula grade C was an independent prognostic factor after multivariate analysis (hazard ratio 2.49; 95% confidence interval 1.56-3.96; P< 0.001). Moreover, independent prognostic significance was also detected for glasgow prognostic score (GPS) 2 (P=0.021), blood transfusion (P< 0.001), International Union Against Cancer (UICC) pT3 or T4(P= 0.003), pathological plexus invasion (P= 0.001), lymph node status (N1) (P= 0.024), no adjuvant therapy (P< 0.001). Furthermore, multivariate analysis demonstrated that independent risk factors for pancreatic fistula grade C was glasgow prognostic score (GPS) 2 (hazard ratio 5.37; 95% confidence interval 1.31-22.0; P=0.019) and male (hazard ratio 6.02; 95% confidence interval 1.77-20.5; P=0.004)

CONCLUSIONS: pancreatic fistula grade C had a significant impact on the long-term survival of patients with pancreatic cancer. The improvement of operative procedure or perioperative management to reduce the incidence of pancreatic fistula grade C may lead to a favorable survival in these patients.

S053 DOES DRAIN FLUID AMYLASE ACCURATELY PREDICT PANCREATIC FISTULA? Christina W Lee, MD, Henry Pitt, MD, Taylor Riall, MD, Sean Ronnekleiv-Kelly, MD, Jacqueline Israel, MD, Glen Leverson, PhD, Abhishek Parmar, MD, Molly E Kilbane, RN, Bruce L Hall, MD, PhD, MBA, Sharon M Weber, MD, University of Wisconsin Hospital and Clinics, Madison, WI; Temple University Health System, Philadelphia, PA; University of Texas Medical Branch, Galveston, TX; Indiana University Health, Indianapolis, IN; Washington University, St. Louis, MO, Madison, US

BACKGROUND/INTRODUCTION: Improvements in the ability to predict pancreatic fistula (PF) could enhance patient outcome by early drain removal and avoidance of drain-related morbidity in those who will not develop PF. Although clinical predictors are associated with an increased risk for PF, these are imprecise. Previous studies have shown that drain fluid amylase on post operative day 1 (DFA1) >5000 is predictive of PF. Therefore, we sought to assess the accuracy of DFA1 to predict PF.



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METHODS: Patients undergoing pancreatic resection from 11/1/11 to 12/31/12 were selected from the American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) Pancreatectomy Demonstration Project (PDP) database. PF was defined as persistent drainage of amylase-rich fluid in addition to drain continuation > 7 days, percutaneous drainage of pancreatic fluid collection, or re-operation. Factors significantly associated with pancreatic fistula on univariate analysis (p < 0.1) were included in logistic regression analysis to evaluate factors independently associated with PF. An ROC curve was utilized to determine the best predictive performance between DFA1 and PF.

RESULTS: DFA1 was recorded in 536 of 2724 patients who underwent PR, including patients undergoing pancreaticoduodenectomy (n=380), distal pancreatectomy (n=140), and enucleation (n=16). PF occurred in 92 subjects (17.2%). On univariate analysis, DFA1, increased body mass index (BMI), small pancreatic duct size and soft pancreatic texture were significantly associated with PF (p < 0.05). On multivariate analysis, all four of these factors were independently associated with PF (p<0.05). Among multiple DFA1 cutoff values, 60 U/L demonstrated the highest sensitivity (Se) and negative predictive value (NPV, Table 1). 141 (26.3%) subjects satisfied this DFA1 cutoff. ROC confirmed the significant relationship between DFA1 and PF, with a c-statistic of 0.761 (Figure 1).

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CONCLUSIONS: Although DFA1 >5000 U/L was associated with high specificity, the sensitivity was low, thus decreasing its clinical usefulness. Lower DFA1 levels resulted in improved NPV; for example, a cut-off of 100 would incur only 4% FN rate while allowing 31% (170/536) of patients to undergo early drain removal safely. Therefore, in patients with low DFA1, early drain removal is recommended.

S054 EARLY DRAIN REMOVAL: THE MIDDLE GROUND BETWEEN THE DRAIN VERSUS NO DRAIN DEBATE IN PATIENTS UNDERGOING PANCREATICODUODENECTOMY. A PROSPECTIVE VALIDATION STUDY Zhi Ven Fong, MD, Camilo Correa-Gallego, MD, Cristina R Ferrone, MD, Gregory R Veillette, MD, Sarah P Thayer, MD, Andrew L Warshaw, MD, Keith D Lillemoe, MD, Carlos Fernandez-del Castillo, MD, Massachusetts General Hospital, Boston, US

INTRODUCTION: Surgeons have been pushing the envelope on abandoning routine intraperitoneal drainage after pancreaticoduodenectomy (PD). We performed an unbiased assessment of drain amylase level as a predictor of pancreatic fistula (PF) development.

METHODS: We prospectively measured daily drain amylase levels, and correlated them with the development of PF in two independent cohorts of patients undergoing PD: training- (n=126; year 2008) and validation-cohort (n=369; years 2009-2012).

RESULTS: First postoperative day (POD 1) drain amylase level had the highest predictive ability (concordance-index: 0.911, figure 1) for development of PF in the training cohort. An amylase level ≥612 showed the best accuracy (86%), sensitivity (93%), and specificity (79%). In the validation cohort, 229 (62.1%) patients had a POD 1 drain amylase level of <600 U/L, and PF developed in only 2 (0.9%) cases, whereas in patients with POD 1 drain amylase level of ≥600 U/L (n=140) the PF rate was 31.4% (OR 52, p<0.0001). On multivariate logistic regression analysis, POD 1 drain amylase level of <600 U/L (p<0.0001) was a stronger predictor of the absence of PF than pancreatic gland texture (OR 5.2, p=0.002) and duct diameter (OR 0.9, p=0.835).

CONCLUSIONS: Following PD, the risk of PF is <1% if POD 1 drain amylase level is <600 U/L. We propose that in this group, which comprise >60% of patients, drains should be removed on POD 1, and are currently validating this strategy.

S055 THE HYSLAR TRIAL: A PROSPECTIVE RANDOMIZED TRIAL ON THE USE OF A RESTRICTIVE FLUID REGIMEN WITH 3% HYPERTONIC SALINE (HS) VERSUS LACTATED RINGERS (LR) IN PATIENTS UNDERGOING PANCREATICODUODENECTOMY (PD) Harish Lavu, MD, Naomi Sell, MHS, Jordan Winter, MD, Timothy Carter, MD, David Maguire, MD, David Gratch, MD, Marian Feil, CRNA, Richard Berman, MD, Zvi Grunwald, MD, Benjamin Leiby, PhD, Edward Pequignot, MS, Ernest Rosato, MD, Charles Yeo, MD, Thomas Jefferson University, Philadelphia, PA, Philadelphia, US

INTRODUCTION: Restrictive fluid regimens have been shown to reduce perioperative complications in patients undergoing surgery. The objective of this study was to determine if the volume and type of fluid administered during and after PD impacts postoperative outcomes.



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METHODS: Between May 2011 and November 2013, patients undergoing PD were consented and enrolled in an IRB approved, prospective, randomized trial (NCT 01428050). At laparotomy, patients were stratified by gland texture (soft vs hard) and randomized to LR (15ml/kg/hr LR intraop, and 2ml/kg/hr LR postop until the morning of POD #1) or HS (9ml/kg/hr LR and 1ml/kg/hr HS intraop, and 1ml/kg/hr HS postop until the morning of POD #1). The trial was powered to detect a 30% reduction in the overall rate of complications (80% power, alpha= 0.05, chi-squared test).

RESULTS: There were 245 patients, with 122 and 123 in the LR and HS groups, respectively. Demographic variables between groups were similar (Table). The LR patients had a significantly greater net fluid balance (91 vs 65 ml/kg, p=0.02) for the entire admission. The overall complication rate (54% vs 41%, p<0.05) and the cumulative number of complications (120 vs 80, p=0.01), were significantly greater in the LR group. Reoperation rate, length of stay, readmission rate, and 30 day mortality were similar between groups.

CONCLUSIONS: A restrictive fluid regimen with 3% HS significantly reduces complications in patients undergoing PD.

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S056 CURRENT MANAGEMENT OF DELAYED BLEEDING AFTER PANCREATICODUODENECTOMY Young Joon Ahn, PhD, Jin He, Jia-hua Leng, John L Cameron, Nita Ahuja, Martin A Makary, Kenzo Hirose, Timothy M Pawlik, Matthew Weiss, Christopher L Wolfgang, Johns Hopkins Medical Institution, Baltimore, US

INTRODUCTION :Delayed bleeding after pancreaticoduodenectomy (PD), defined as bleeding after post-operative day 5, is a rare but life threatening complication. Options for management include angiography with embolization, endoscopic procedures, supportive therapy or re-operation. However, the optimal management remains unclear. We summarized our experience on the management of delayed bleed in order to better define the outcomes associated with different types of management.

PATIENTS & METHODS :The electronic records of 4513 patients who underwent pancreaticoduodenectomy between October 1987 and July 2013 were analyzed regarding postoperative bleeding complications.

RESULTS :Delayed bleeding occurred in 86 patients (1.9 %) following pancreaticoduodenectomy (classical PD: 48, pylorus preserved PD: 38) with median time of occurrence of 12.5 days from operation (range: 5 to 96). The pattern of bleeding was classified into intraluminal bleeding only (n=51; 59.3%) extraluminal bleeding only (n=22; 26.6%), and both (n=13; 15.1%). Within this cohort, 50 patients (58.1%) had an associated postoperative pancreatic fistula (ISGPF grade A: 5, B: 26, C: 19). The majority of delayed bleeding was the result of a pseudoaneurysm (n=40, 46.5%), while other sources included suture lines (n=12), marginal ulcer or gastritis (n=12), drain-related bleeding (n=5), others (n=5) and unknown cause (n=12). A total of 82 angiographies were performed in 65 patients (65/86:75.6) The embolization was performed in 44 patients. Immediate control of bleeding was achieved in 32 cases (72.7%) with coil embolization or covered stent insertion. Of those patients who failed initial embolization, 9 cases with ongoing bleeding were explored surgically and 3 underwent repeated angiography with re-embolization. Among these 3 patients, 2 survived and 1 died. As for pseudoaneurysmal bleeding, 27 of 39 patients who attempted angiography first achieved effective bleeding control with embolization and 4 cases were controlled by surgery. Endoscopy found bleeding focus in 18 out of 44 patients (41%) who underwent endoscopy and 13 hemodynamically stable patients were clipped and cauterized subsequently. Other 5 patients underwent exploration for ongoing bleeding after endoscopy. Surgery was attempted in total 21 patients to control bleeding and 11 of the 21 patients survived eventually. 6 patients were explored as 1st line treatment and 4 patients survived. The other 10 patients with delayed bleeding were managed conservatively. Overall mortality was 18.6 % (16 / 86).

CONCLUSIONS :Delayed bleeding after pancreatic surgery should prompt the suspicion of a pseudoaneurysm even in intraluminal bleeding only. Angiography with embolization showed better outcome as 1st line approach for urgent bleeding suspicious of pseudoaneurysm. For patients with pseudoaneurysm, operative



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exploration should be reserved for unstable patient or failed angiographic intervention. Endoscopy seems to play minimal role in urgent bleeding.

S057 BILE-CULTURE BASED ANTIMICROBIAL PROPHYLAXIS REDUCES SURGICAL SITE INFECTIONS (SSIS) IN PANCREATIC SURGERY Alessandro Zerbi, MD, Maria Rachele Angiolini, MD, Francesca Gavazzi, MD, Cristina Ridolfi, MD, Paola Morelli, MD, Erminia Casari, MD, Maria Carla Tinti, MD, Marco Montorsi, MD, Section of Pancreatic Surgery, Department of Surgery; Infectious Diseases Unit, Hospital Health Direction; Humanitas Research Hospital, Rozzano, Milan, Italy. University of Milan School of Medicine, Milan, Italy, Rozzano (mi), IT

BACKGROUND: Cefazolin is widely accepted as antimicrobial prophylaxis in hepato-bilio-pancreatic surgery. Microbial resistance to this drug is rapidly increasing, nullifying the expected beneficial effects of its administration and exposing patients to potentially severe SSIs.

Aim of this study is definition of an alternative prophylaxis schedule targeted on bile cultures and validation of its efficacy on SSIs incidence among patients undergoing pancreatic surgery in a referral centre.

METHODS: Between Jan-2010 and Oct-2013 we performed 222 consecutive pancreatic resections requiring bile contamination (203 pancreaticoduodenectomies and 19 total pancreatectomies). We routinely performed culture on bile samples obtained intra-operatively and we prospectively recorded SSIs development. Analyzing antimicrobial susceptibility of detected germs, we introduced from Mar-2013 ampicillin-sulbactam as alternative to standard cefazolin for perioperative prophylaxis; we therefore realized a comparison between patients receiving standard (n=170) and new (n=52) schedule.

RESULTS: Analyzing the standard group, 56% of patients had positive bile cultures; the great majority of microbes belonged to Enterococcus Spp. (E. Faecalis 29%, E. Facium 18%). In 47% of patients a preoperative biliary stent was present: it was strongly associated with bile infection (100% vs 17%, p<0,001); bile infection was associated with higher morbidity both in patients with (72% vs 56%, p=0,037) or without stent (87% vs 56%, p=0,026), as well as with higher SSIs rate (63% vs 37%, p=0,113). 49,5% of infected bile samples harbored microbes resistant to cefazolin: in these patients postoperative global SSIs were higher (71% vs 30%, p=0,023) as well as superficial SSIs, deep SSIs and organ-space SSIs. Since we administered ampicillin-sulbactam as perioperative prophylaxis, we observed a significant decrease of superficial (20,6% vs 3,8%, p=0,005) and deep (8,8% vs 0, p=0.025) SSIs, while we noted no difference in organ/space SSIs.

CONCLUSION: Bile infection in pancreatic surgery is related to a significant increase of postoperative morbidity. The choice of ampicillin-sulbactam prophylaxis, based on bile-cultures results, seems useful in reducing SSIs.

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S058 IT IS QUALITY AND QUANTITY: A SINGLE INSTITUTION’S EXPERIENCE IN QUALITY MEASURES OF PANCREATIC CANCER CARE Melanie Ongchin, MD, Jennifer Steve, BS, David Bartlett, MD, Kenneth Lee, MD, Haroon Choudry, MD, Wallis Marsh, MD, Allan Tsung, MD, Zureikat Amer, MD, Zeh Herbert, MD, Hogg Melissa, MD, University of Pittsburgh, Pittsburgh, US

BACKGROUND: Despite extensive analysis of the management of pancreatic cancer care, outcomes vary among institutions. Bilimoria et al developed a set of 50 quality indicators (QI) addressing 5 domains in pancreatic cancer care. We examined our institution’s compliance with these cancer care quality indicators, hypothesizing that tracking these measures would be feasible and would assure high compliance.

METHODS: In 2011, we developed a database for a Pancreatic Quality Improvement Project prospectively maintained to track these QI. We examined patients from April 2011 to July 2012 with pancreatic adenocarcinoma.

RESULTS: 570 patients were captured, 322 had pancreatic adenocarcinoma. Of those patients, 125 were resectable, 25 locally advanced, and 197 metastatic. 26% of patients enrolled in one of our 11 clinical trials. We were >90% compliant with 42 of 43 of the validated QI. Compliance on QI #26 was 86% (table). Median time from diagnosis to surgery was 24 days. 67% received neoadjuvant therapy; median time to treatment (MTTT) was 22 days. 74% received adjuvant therapy; MTTT was 51 days. Of patients who received treatment more than 60 days from diagnosis, 55% were stage 4 deciding on therapy vs hospice. Surgical outcomes tracked include: 2.2% peri-operative mortality, 85% R0 resection, 20.5 median lymph nodes, 350cc median EBL, 459min median OR time, and 34% readmission rate. Our composite score was 9 out of 10 compared to a median of 4 in Bilimoria’s study. One person maintains this database, averaging 8hrs/wk.

CONCLUSION: We adhere to 98% of the validated indicators. Time maintaining this database is minimal and prospectively tracks our performance in pancreatic cancer care. Institutions performing pancreatic surgery should track these indicators as part of their outcomes.

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S059 MOBILE RISK CALCULATOR APP FOR OPERATIVE AND ONCOLOGIC OUTCOMES IN PATIENTS CONSIDERING PANCREADICODUODENECTOMY FOR PANCREATIC ADENOCARCINOMA Pragatheeshwar Thirunavukarasu, MD, Kristopher Attwood, Steven Nurkin, MD, Roswell Park Cancer Institute, Buffalo, US

INTRODUCTION: Accurate assessment of surgical risk prior to pancreaticoduodenectomy is difficult. Procedure-specific and patient related factors such as age and comorbid status make the prediction of operative outcomes subjective, and often inaccurate. Oncological outcomes also depend upon various tumor-specific factors. Use of elaborate scoring systems and nomograms are time consuming and impractical for quick instant use. Tools to provide reliable quantitative information on short and long-term outcomes, as well as risks patients may expect with treatment, may help them deal with these difficult life changing decisions. We aimed to develop a web and mobile application for rapid point-of-care surgical risk and oncological outcome assessment.

METHODS: Using the 1998-2011 National Cancer Database Participant Use File (NCBD-PUF), we identified individual patient and cancer specific variables to risk stratify patients who underwent pancreaticoduodenectomy for pancreatic adenocarcinoma. In a separate analysis, we used the National Surgical Quality Improvement Project of the American College of Surgeons (ACS-NSQIP) database (2005-2012) to extract data on demographic, clinical, operative and postoperative outcome variables on all patients undergoing pancreaticoduodenectomy for cancer. Statistical analyses were performed using a combination of univariate associations and multivariate analyses associated with assessed outcomes. Combining these robust databases and using appropriate statistical validation, we generated user friendly, point of care, clinical calculators to predict risk of operative morbidity and long-term oncologic survival. We then developed web-based mobile apps to make this calculator convenient and user friendly for clinical use.

RESULTS: A mobile application was developed as shown in the attached screen shot. It generates instant output to display surgical risk such as mortality, overall morbidity and serious morbidity (sMorbidity). The application also analyzed stored NSQIP data to calculate the accurateness of the generated predicated outcomes. In a separate calculator (not shown), 1 and 3 year survival data is calculated based on individual clinicopathologic variables.

CONCLUSION: This Point-of-Care Operative and Oncologic Risk Calculator for pancreaticoduodenectomy is a combined NSQIP-NCDB based, easy-to-use application and is compatible with widely used personal and corporate mobile devices. It enables the surgeon to provide patients and families an objective, immediate, point-of-care operative risk assessment, with the accompanied predicted oncologic survival benefit. This would help the surgeon in setting realistic expectations to patients considering surgery, and strengthen the process of informed consent. Our next step would be to prospectively validate the use of this application in the clinical setting.



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S060 PREDICTORS OF EARLY READMISSION AFTER PANCREATECTOMY Jeffrey T Tosoian, MD, MPH, Caitlin W Hicks, MD, MS, Vicente Valero III, MD, John L Cameron, MD, Martin A Makary, MD, MPH, Kenzo Hirose, MD, Frederic E Eckhauser, MD, Nita Ahuja, MD, Timothy M Pawlik, MD, MPH, Matthew J Weiss, MD, Christopher L Wolfgang, MD, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, Baltimore, US

Introduction:/BACKGROUND: There are limited data exploring readmission associated with complex surgical diagnoses. Existing studies frequently underestimate readmission rates because not all patients present to the index hospital where their procedure was performed. We studied the detailed pattern and characteristics of readmission following pancreatectomy at a single institution using a statewide database to improve readmission capture.

METHODS: Using a prospectively-collected institutional database in conjunction with Maryland statewide data, we reviewed pancreas resections performed at the Johns Hopkins Hospital between 2005 and 2010. Only Maryland residents were included in order to capture readmissions to any Maryland hospital.

RESULTS: Of 595 subjects eligible for early readmission, 134 (22.5%) were readmitted to either our institution (n=105, 78.4%) or an outside institution (n=29, 21.6%). The majority (54.5%) of patients were readmitted due to surgical complications, including abdominal abscess, pancreatic fistula, gastrointestinal bleed, urinary tract infection, or respiratory failure. Other

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common reasons for readmission were failure to thrive (11.2%), abdominal pain (9.7%), and gastrointestinal obstruction (6.0%). Patients readmitted for surgical complications were more likely to present to our institution (Fisher’s exact test, P=0.001), while the site of readmission did not differ significantly among other readmission diagnoses. On multivariate analysis, factors associated with readmission included age ≥65, baseline chronic liver disease, undergoing distal pancreatectomy, post-operative intravenous antibiotics, and post-operative drain placement (Table). On Kaplan-Meier analysis, readmitted subjects demonstrated shorter median survival than those who were not readmitted (20.3 versus 23.1 months, log-rank test P=0.011).

DISCUSSION/CONCLUSION: Early readmission after pancreatectomy is common and a significant predictor of decreased overall survival. Specific patient-level factors may identify patients at increased risk of readmission. Whether high-risk patients could be targeted for risk-reduction strategies that .would decrease readmissions and possibly lower hospital costs deserves further consideration.

S061 HIGH-VOLUME SURGEONS VERSUS HIGH-VOLUME HOSPITALS: ARE BEST OUTCOMES MORE DUE TO WHO OR WHERE? Paul G Toomey, MD, Sharona B Ross, Amanda E Igartua, Michael DeGori, Anthony F Teta, Kenneth Luberice, Prashant B Sukharamwala, MD, Alexander S Rosemurgy, MD, Florida Hospital Tampa, Tampa, US

INTRODUCTION: High-volume hospitals are purported to provide ‘best’ outcomes. High-volume hospitals and high-volume surgeons are inextricably related. We undertook this study to evaluate the outcomes after pancreaticoduodenectomy when high-volume surgeons relocate to a low-volume hospital.



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METHODS: Outcomes after the last 50 pancreaticoduodenectomies at a high-volume hospital in 2012 were compared to the outcomes after the first 50 pancreaticoduodenectomies undertaken at a low-volume (i.e., no pancreaticoduodenectomies in >5 years) hospital in 2012-13; all operations were undertaken by the same surgeons. Data are presented as median (mean ± SD).

RESULTS: Patients undergoing pancreaticoduodenectomies at a high-volume vs. a low-volume hospital were not different relative to sex and age (Table). Patients operated upon at the low-volume hospital had lower ASA class, had shorter operations with less blood loss, spent less time in the ICU, and had shorter length of stay (p < 0.05 for each, Table); 30-day mortality and 30-day readmission rates were not different (Table).

CONCLUSIONS: The salutary benefits of being a high-volume hospital for pancreaticoduodenectomy are transferred to a low-volume hospital when high-volume surgeons relocate. The ‘best’ outcomes associated with high-volume hospitals may be primarily due to the high-volume surgeons who work there, and the ‘best’ results follow the high-volume surgeons. The ‘best’ results seem to be related more to who does the pancreaticoduodenectomy rather than where the pancreaticoduodenectomy is undertaken.

S062 WHAT ARE THE FINANCIAL IMPLICATIONS OF CENTERS FOR REGIONAL HEALTHCARE? Alexander S Rosemurgy, MD, Richard L Klein, Carrie E Ryan, MS, Prashant B Sukharamwala, MD, Thomas W Wood, MD, Sharona B Ross, MD, Florida Hospital Tampa, Tampa, US

INTRODUCTION: Financial implications on regionalization of healthcare and programmatic development are not often considered. We undertook this study to evaluate and compare hospital cost of care and income with a common operation (laparoscopic cholecystectomy) versus an operation often associated with HPB programmatic development and healthcare regionalization (pancreaticoduodenectomy).

METHODS: The charges and reimbursements of all laparoscopic cholecystectomies (n=201) and pancreaticoduodenectomies (n=44) at one hospital undertaken from

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June 2012 to June 2013 were determined. Comparisons were undertaken using ANOVA with significance accepted at p ≤ 0.05. Data are reported as median data or as median (mean ± SD).

RESULTS: Pancreaticoduodenectomy, relative to laparoscopic cholecystectomy, had greater time in the operating room (283 min vs. 93 min), hospital charges ($108,040.87 vs. $25,055.85), and hospital costs ($15,482.15 vs. $3,453.78) (p<0.0001 for each), but generated similar income ($2,480.23 vs. $3,058.83, p=0.88).

CONCLUSIONS: Pancreaticoduodenectomy requires more resource allocation and costs hospitals more but leads to no more income. Many hospitals invest great effort and resources to build programs and centers for regional healthcare. However, their accounting systems are not based on cost accounting, but rather on complex formulas of cost allocation. Consequently, these accounting systems have great, and possibly inappropriate, impact on perceived income associated with care. Considering these systems, it seems hospitals derive more return on investment from commonly undertaken operations than those often associated with regionalization of healthcare and programmatic development. Accounting systems need to reflect actual costs to allow determinations of actual income to better allocate healthcare resources and to seek appropriate compensation for hospital care.



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S063 THE INCIDENCE OF PANCREATOGENIC DIABETES AFTER MAJOR PARTIAL PANCREATIC RESECTION MAY BE GREATER THAN YOU THINK Richard A Burkhart, MD, Susan M Gerber, MD, Renee M Tholey, MD, Kathleen Lamb, MD, Anitha Somasundaram, MD, Caitlin McIntyre, Eliza Fradkin, Annie Ashok, Robert Felte, MD, Jaya Mehta, Ernest Rosato, MD, Harish Lavu, MD, Serge A Jabbour, MD, Charles J Yeo, MD, Jordan M Winter, MD, Department of Surgery, Jefferson Pancreas, Biliary, and Related Cancer Center, Thomas Jefferson University, Philadelphia, PA; Department of Endocrinology, Thomas Jefferson University Hospital, Philadelphia, PA, Philadelphia, US

BACKGROUND: The number of pancreatic resections performed each year in the US estimated at 5000 patients and growing. With many performed for benign disease, many patients will experience prolonged survival (>2 years), yet the long-term risk of pancreatogenic (type III) diabetes remains unknown. Previous estimates from small studies outside the U.S. suggest a risk of developing diabetes between 10-20%.

METHODS: A total of 1107 patients underwent pancreatectomy at Thomas Jefferson University between 2005 and 2012. After IRB approval, attempts were made to contact all living patients by telephone. Pre- and postoperative diagnoses of diabetes mellitus (DM) were confirmed by verbal questionnaire. Individuals who completed the diabetes-focused survey were included.

RESULTS: Telephone calls were made to 691 living patients who underwent partial pancreatectomy. Diabetes-specific information was successfully obtained for 257 patients (representing 23% of the total cohort), including 179 who underwent pancreaticoduodenectomy (PD) and 78 who underwent distal pancreatectomy (DP). The median follow-up time after resection was 2.1 years.

In the PD group: 44 (25%) patients reported having DM prior to resection (median 7 years prior, range 0.1 to 30), with 10 (6%) reporting onset within 1 year. Of the group carrying a pre-operative diagnosis of DM, 3 (7%) had improved glucose control after resection (dose reduction in diabetes medicines), while 21 (48%) required escalated management. Out of 135 patients without preoperative DM, 24 (18%) were newly diagnosed with DM postoperatively (median onset 7.5 months postoperatively, range 1-64).

In the DP group: 23 patients (29%) had DM preoperatively, with just 4 having onset within 1 year of resection (5%). No patients had improved glucose control after resection, while 6 (26%) patients carrying a preoperative diagnosis of DM had worse control after resection. Out of 55 patients without preoperative DM, 17 (31%) developed new onset DM after resection (median 6 months, range 0-60).

In the total cohort after partial pancreatectomy, 26% either experienced worse glucose control (27 of 67 with preop DM, 40%) or a new diagnosis of DM (41 of 190 without preop DM, 22%). A high preoperative HgbA1C level (>6%) was associated with an increased risk of developing new-onset DM post-resection (38% in the >6% HgbA1C group vs. 11%, p<0.02).

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ORAL ABSTRACTS

CONCLUSIONS: Twenty-two percent of patients undergoing partial pancreatectomy experience new onset DM and 40% of patients experience worsening DM after resection, a higher percentage of patients than previously reported. These figures likely underestimate the true lifetime risk of pancreatogenic diabetes, in light of the short follow-up time in this patient cohort (2.1 years). An elevated preoperative HgbA1C (>6%) identifies patients at highest risk for developing new onset DM after resection.

S064 EFFECT OF HIGH-DOSE PANCREATIC ENZYME REPLACEMENT THERAPY ON THE DEVELOPMENT OF NON-ALCOHOLIC FATTY LIVER DISEASE AFTER PANCREATICODUODENECTOMY, PAYING ATTENTION TO ETIOLOGY OF DISEASES AND THE REMNANT PANCREATIC VOLUME Rie Sato, Masashi Kishiwada, Yasuhiro Murata, Akihiro Tanemura, Naohisa Kuriyama, Yashinori Azumi, Shugo Mizuno, Masanobu Usui, Hiroyuki Sakurai, Masami Tabata, Shuji Isaji, Hepatobiliary Pancreatic and Transplant Surgery, Mie University School of Medicine, Tsu Mie, JP

BACKGROUND: Conventional nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are characterized by two steps of intrahepatic lipid accumulation and inflammatory progression to fibrosis. The high incidence of NAFLD after pancreaticoduodenectomy (PD) has been recently known, suggesting the effect of malnutrition due to pancreatic exocrine deficiency (Kato H, Isaji S, J Hepatobiliary Pancreat Sci 2010). The aim of this study is to investigate whether high-dose pancreatic enzyme replacement therapy can prevent the development of NAFLD after PD, paying attention to etiology of diseases and the remnant pancreatic volume(RPV) measured by CT volumetry.

PATIENTS AND METHODS: Among the consecutive 183 patients who underwent PD from April 2007 to March 2013, we retrospectively reviewed the charts of 144 patients who had been followed up more than 6 months after PD. The indication of PD was pancreatic carcinoma(n=77), IPMN(n=26), bile duct carcinoma (n=12), ampullary carcinoma (n=9), other neoplasm (n=9) and others (n=11). From October 2011, we have performed high-dose pancreatic enzyme replacement therapy from early postoperative days using enteric-coated, delayed-release pancrelipase (1800mg/day), and the subjects could be classified into the two periods: early period (from April 2007 to September 2011, n=93) and late period (from October 2011 to March 2013, n=51). In early period, mean dose of pancreatic enzyme was pancreatine 6.43g/day at 1 month after PD.



ORAL ABSTRACTS

RESULTS: NAFLD was found in 54 patients (37.5%), 83% of whom developed it within 3 months after operation. Chronological data (preoperative and at 1, 3, 6 and 12 months after PD) of serum albumin were 3.6, 3.1, 3.4, 3.6 and 3.6 g/dl in early period and 3.9, 3.4, 3.7, 3.8 and 3.9 g/dl in late period, showing significantly higher levels at 1, 3 and 12month in late period (p<0.05). Total cholesterol levels did not differ significantly. The incidence of NAFLD was lower in late period (29.4%) than in early period (41.9%), not showing significant difference (p=0.138). In the patients with pancreatic carcinoma (n=77: mean RPV of 10.03ml), the incidence of NAFLD was not significantly different between the two periods: 42.0% vs. 39.0% (p=0.815), while, in the patients without pancreatic carcinoma (n=67: meanRPV of 22.07ml), the incidence of NAFLD is significantly lower in late period than in early period: 41.9% vs.17.4% (P=0.045). In the patients with pancreatic carcinoma, the incidence of diarrhea in postoperative day 30 is extremely high, showing no significant difference between the two periods: 56.0% vs. 66.7% (p=0.362), while, in the patients without pancreatic carcinoma, the incidence of diarrhea was much lower in late period compared to early period: 32.6% vs. 13.0% (p=0.084). By multivariate analysis including perioperative various factors, female, postoperative diarrhea and age were selected as the independent risk factor for NAFLD.

CONCLUSION: High-dose pancreatic enzyme replacement therapy after PD significantly prevented the development of NAFLD after PD, especially in the patients without pancreatic adenocarcinoma. The significantly higher incidence of diarrhea in the patients with pancreatic carcinoma, which was due to nerve plexus dissection around SMA and smaller remnant pancreatic volume, was considered to disturb the effect of high-dose enzyme therapy.

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2014 Membership Roster

2014 MEMBERSHIP ROSTER2014 MEMBERSHIP ROSTER

A. Saavedra, Juan R., MD INACTIVE | 2011 Cleveland Clinic Foundation Email: [email protected]

Abbasi, Ammara, MD RESIDENT | 2014 Beth Israel Deaconess Medical Center Address: 110 Francis St., Suite 9B Boston, MA 02215 Email: [email protected]

Abbott, Daniel E., MD ACTIVE | 2014 Univ. of Cincinnati Surgery Address: 3156 Wolf Run Ct. Cincinnati, OH 45244 Email: [email protected]

Abood, Gerard, MD ACTIVE | 2013 Loyola Univ. Medical Center Address: 2160 S. First Ave. Maywood, IL 60153 Email: [email protected]

Abraham, Anasooya, MD INACTIVE | 2011 Univ. of Minnesota Email: [email protected]

Adam, Ulrich, MD ACTIVE | 2014 Vivantes Humbolt Klinikum Berlin Dept. of General and Vascular Surgery Address: Am Nordgraben 2 Berlin, 13509 Germany Email: [email protected]

Adams, David, MD ACTIVE | 2014 MUSC Medical Center Dept. of Surgery Address: 25 Courtenay Dr., MSC 290 Charleston, SC 29425 Email: [email protected]

Ahmad, Syed A., MD ACTIVE | 2014 Univ. of Cincinnati Medical Center Surgical Oncology Address: 231 Albert Sabin Way, ML 0772 Cincinnati, OH 45267 Email: [email protected]

Ahmed, Shuja, MD RESIDENT | 2014 Wake Forest Baptist Medical Center Dept. of Surgery Address: Medical Center Blvd. Winston Salem, NC 27157 Email: [email protected]

Ahmed Ali, Usama, MD RESIDENT | 2014 AMC Amsterdam Address: Meibergdreef 9, Amsterdam, 1105 AZ Netherlands Email: [email protected]

Ahn, Young Joon, MD, PhD ACTIVE | 2014 Johns Hopkins Medical Institute Address: 17 Mica Court Baltimore, MD 21209 Email: [email protected]

Ahuja, Nita, MD ACTIVE | 2014 Johns Hopkins Univ. Surgical Oncology Address: 600 Wolfe St. Baltimore, MD 21287 Email: [email protected]

Albagli, Rafael, MD ACTIVE | 2013 National Cancer Institute of Brazil Address: Munig Baruto 396 11002 Rio de Janeiro, Brazil Email: [email protected]

Ali, Naoman, MD INACTIVE | 2011 Beaumont Hospital Email: [email protected]

Allen, Peter J., MD INACTIVE | 2010 Memorial Sloan-Kettering Cancer Center Email: [email protected]

Allendorf, John, MD ACTIVE | 2014 Winthrop Address: 120 Mineola Blvd. Mineola, NY 11501 Email: [email protected]


TABLE OF CONTENTS2014 Membership Roster

2014 MEMBERSHIP ROSTER

Alrefaie, Waddah, MD INACTIVE | 2011 Univ. of Minnesota Email: [email protected]

Alsfasser, Guido, MD ACTIVE | 2014 Univ. of Rostock Dept of Surgery Address: Schillingallee 35 Rostock, 18057 Germany Email: [email protected]

Amini, Albert RESIDENT | 2014 Medical College of Wisconsin Address: 9200 W Wisconsin Ave. Milwaukee, WI 53226 Email: [email protected]

Andersen, Dana, MD ACTIVE | 2014 Digestive Disease Division / NIDDK / NIH Address: 6707 Democracy Blvd., Rm 659 Bethesda, MD 20892 Email: [email protected]

Androutsopoulos, Vasiliki INACTIVE | 2009 Email: [email protected]

Angst, Eliane, MD INACTIVE | 2009 Email: [email protected]

Antiporda, Michael, MD RESIDENT | 2014 Mayo Clinic Jacksonville Address: 4500 San Pablo Rd. Jacksonville, FL 32224 Email: [email protected]

Arafat, Hwyda, MD, PhD INACTIVE | 2010 Thomas Jefferson Univ. Email: [email protected]

Aranha, Gerard, MD ACTIVE | 2014 Loyola Univ. Medical Center Dept. of Surgery Address: 2160 S First Ave. Maywood, IL 60523 Email: [email protected]

Arcangeli, Annarosa, MD, PhD ACTIVE | 2013 Univ. of Florence Experimental Pathology and Oncology Address: Viale G.B. Morgagni 50 Firenze, 50134 Italy Email: [email protected]

Arcerito, Massino, MD RESIDENT | 2013 Univ. of Michigan Surgery Address: 1500 E Medical Center Dr., SPC 534 Ann Arbor, MI 48109-5343 Email: [email protected]

Arimoto, Jun, MD RESIDENT | 2013 Yokohama City Univ. Address: Kinko-cho 8-1-1004 Yokohama City, Japan Email: [email protected]

Arnoletti, Pablo, MD ACTIVE | 2013 Florida Hospital Address: 2415 N Orange Ave., Suite 400 Orlando, FL 32714

Arous, Edward, BS INACTIVE | 2011 Univ. of Massachusetts Medical School Email: [email protected]

Arrangoiz, Rodrigo INACTIVE | 2012 Email: [email protected]

Arrese, David, MD INACTIVE | 2012 Riverside Methodist Hospital Email: [email protected]

Asai, Kengo, MD RESIDENT | 2014 Mayo Clinic Address: 200 First St. SW, Rochester, MN 55901 Email: [email protected]

Asano, Takedhe, MD INACTIVE | 2009 Teikyo Univ. SOM Email: [email protected]

109



Asbun, Horacio, MD ACTIVE | 2014 Mayo Clinic Dept. of Surgery Address: 4500 San Pablo Rd. Jacksonville, FL 32224 Email: [email protected]

Ashley, Stanley, MD ACTIVE | 2013 Brigham & Women’s Hospital Dept. of Surgery Address: 75 Francis St. Boston, MA 02115 Email: [email protected]

Assifi, Mura, MD RESIDENT | 2013 Email: [email protected]

Atkinson, Donald, MD ACTIVE | 2013 Allegheny General Hospital Dept. of Surgery Address: 420 E. North Ave., Suite 304 Pittsburgh, PA 15212 Email: [email protected]

Atwal, Tegpal, MD RESIDENT | 2013 Mayo clinic, Rochester Gastroenterology Address: 93 Grande Isle Ave. SW, Unit 2513 Rochester, MN 55902 Email: [email protected]

Avery, Nathan, MD RESIDENT | 2014 Virginia Mason Medical Center Address: 1105 Spring St., Apt. 1302 Seattle, WA 98104 Email: [email protected]

Azih, Lilian INACTIVE | 2012 Email: [email protected]

Babicky, Michele INACTIVE | 2012 Email: [email protected]

Baker, Marshall S., MD, MBA ACTIVE | 2014 NorthShore Univ. Health System Dept. of Surgery Address: Walgreen’s Building 2nd Floor 2650 Ridge Ave. Evanston, IL 60201 Email: [email protected]

Bakker, Olaf, MD INACTIVE | 2010 Univ. Medical Center Utrecht Email: [email protected]

Ball, Chad, MD, MSc, FRCSC, FACS ACTIVE | 2014 Univ. of Calgary Surgery Address: 3538 - 8th Ave. N.W. Calgary, AB T2N 1C9 Canada Email: [email protected]

Ballehaninna, Umashankar, MD RESIDENT | 2013 Maimonides Medical Center Surgery Address: 4802 10th Ave., 4th Fl. Brooklyn, NY 11219 Email: [email protected]

Bang, Ji Young, MD, MPH RESIDENT | 2013 Univ. of Alabama at Birmingham Birmingham, AL Email: [email protected]

Banks, Peter A., MD ACTIVE | 2014 Brigham & Women’s Hospital Clinical Gastroenterology Address: 75 Francis St. Boston, MA 02115 Email: [email protected]

Barboza, Eduardo, MD ACTIVE | 2013 Clinica San Felipe Surgery Address: Gregorio Escobedo 676, 411 4th Fl. Lima, 00011 Peru Email: [email protected]




Barnett, Jr., Carlton C., MD INACTIVE | 2010 Denver Health/Univ. of Colorado Email: [email protected]

Barringer, Jennifer, MS, PA-C INACTIVE | 2011 UPMC Email: [email protected]

Barron, Morgan, MD RESIDENT | 2013 Indiana Univ. School of Medicine Address: 545 Barnhill Drive, EH-125 Indianapolis, IN 46202 Email: [email protected]

Barry, Linda, MD INACTIVE | 2010 Univ. of South Florida Email: [email protected]

Barton, Joshua, MD INACTIVE | 2012 Mayo Clinic Email: [email protected]

Baschnagel, Andrew, MD RESIDENT | 2014 William Beaumont Hospital Address: 3601 W 13 Mile Rd. TROY, MI 48073 Email: [email protected]

Bass, Barbara, MD INACTIVE | 2009 Email: [email protected]

Bassi, Claudio, MD ACTIVE | 2014 University of Verona Surgery and Oncology Address: Hospital G.B. Rossi Verona, 37134 Italy Email: [email protected]

Baumgartner, Joel, MD INACTIVE | 2011 Univ. of Pittsburgh Medical Center Email: [email protected]

Bausch, Dirk, MD ACTIVE | 2014 UK-SH, campus Lübeck General & Visceral Surgery Address: Ratzeburger Allee 160 Lübeck, 23538 Germany Email: [email protected]

Beane, Joal, MD INACTIVE | 2011 Indiana Univ. Email: [email protected]

Behrman, Stephen, MD ACTIVE | 2014 Univ. of Tennessee, Memphis Dept. of Surgery Address: 910 Madison Ave. #208 Memphis, TN 38163 Email: [email protected]

Behrns, Kevin E., MD ACTIVE | 2014 Univ. of Florida Dept. of Surgery Chairman Address: PO Box 100286, 1600 SW Archer Rd., Room 6174 Gainesville, FL 32607 Email: [email protected]

Benarroch-Gampel, Jaime INACTIVE | 2012 Email: [email protected]

Benson, Douglas, MD INACTIVE | 2010 Univ. of Colorado Email: [email protected]

Bentrem, David J., MD INACTIVE | 2011 Northwestern Univ. Medical School Email: [email protected]

Berger, Adam INACTIVE | 2009 Thomas Jefferson Univ. Email: [email protected]

Berri, Richard, MD INACTIVE | 2010 MD Anderson Cancer Center Email: [email protected]

111



Besselink, Marc, MD, MSc, PhD ACTIVE | 2014 Academic Medical Center Amsterdam Address: Meibergdreef 9, Room G4.196 Amsterdam, 1105 AZ Netherlands Email: [email protected]

Bever, Katherine, MD INACTIVE | 2010 Univ. of Maryland Email: [email protected]

Bey, Eric PhD INACTIVE | 2009 Email: [email protected]

Biehl, Thomas, MD INACTIVE | 2012 Virginia Mason Medical Center Email: [email protected]

Bildzukewicz, Nikolai, MD INACTIVE | 2009 Thomas Jefferson Univ. Hospital Email: [email protected]

Binkley, Charles E., MD ACTIVE | 2013 Kaiser Permanente San Francisco Medical Center Surgery Address: 2238 Geary Blvd. San Francisco, CA 94115 Email: [email protected]

Bliss, Lindsay, MD RESIDENT | 2014 Beth Israel Deaconess Medical Center Address: 330 Brookline Ave., Stoneman 9 Attn: Jennifer Tseng Boston, MA 02215 Email: [email protected]

Bloomston, Mark, MD INACTIVE | 2009 Ohio State Univ. Email: [email protected]

Bock, Eileen BE INACTIVE | 2011 Loyola Univ. Medical Center Email: [email protected]

Boggi, Ugo, MD ACTIVE | 2014 Oredale Di Cisanello Divisione Di Chirurgia General Address: Via Paradisa, 2 Pisa, 56124 Italy Email: [email protected]

Boja-Cacho, Daniel INACTIVE | 2009 Email: [email protected]

Bold, Richard J., MD INACTIVE | 2011 UC Davis Cancer Center Email: [email protected]

Bollen, Thomas, MD INACTIVE | 2009 St. Anthonys Hospital Email: [email protected]

Bolton, Nathan, MD RESIDENT | 2014 Ochsner Clinic Foundation Address: 1542 Jefferson Highway New Orleans, LA 70121 Email: [email protected]

Bonwense, Stefan INACTIVE | 2012 Email: [email protected]

Boone, Brian, MD RESIDENT | 2014 Univ. of Pittsburgh Medical Center Address: 1409 4th St. Pittsburgh, PA 15221 Email: [email protected]

Booy, Stephanie Msc RESIDENT | 2013 Erasmus MC Internal Medicine and Surgery Rotterdam, Netherlands Email: [email protected]

Borzomati, Domenico, MD, PhD, FACS INACTIVE | 2013 Policlinico Universitario Campus Biomedico Email: [email protected]




Boutros, Cherif, MD, MSc ACTIVE | 2014 Univ. of Maryland School of Medicine General and Oncologic Surgery Address: 22 S Greene St., Room S4B12 Baltimore, MD 21201 Email: [email protected]

Bouvet, Michael, MD ACTIVE | 2013 Univ. of California, San Diego Moores Cancer Center Address: 3855 Health Sciences Drive La Jolla, CA 92093-0987 Email: [email protected]

Boyd, Casey, MD INACTIVE | 2012 Univ. of Texas Medical Branch Email: [email protected]

Bradley, III, Edward, MD INACTIVE | 2011 Florida State Univ. College of Medicine Email: [email protected]

Brat, Gabriel, MD INACTIVE | 2009 Johns Hopkins Hospital Email: [email protected]

Brentnall, Teresa, MD HONORARY/SPEAKER | 2012 Univ. of Washington Address: 1959 NE Pacific St., Box 356424 Seattle, WA 98195 Email: [email protected]

Bressan, Alexsander, MD RESIDENT | 2014 Foothills Medical Centre - Univ. of Calgary Address: 2010, Ulster Rd. NW, Unit 308 Calgary, AB T2N2T9 Canada Email: [email protected]

Brijbassie, Alan A., MD INACTIVE | 2012 Univ. of Virginia Email: [email protected]

Brisinda, Giuseppe, MD ACTIVE | 2013 Catholic Univ. Hospital “Agostino Gemelli” Surgery Address: Largo Agostino Gemelli 8 Rome, 00168 Italy Email: [email protected]

Brody, Jonathan, MD ACTIVE | 2013 Jefferson Medical College Dept. of Surgery Address: 1025 Walnut St., Suite 623 Philadelphia, PA 19107 Email: [email protected]

Broniatowski, Sharon ACTIVE | 2014 Cleveland Clinic General Surgery Address: 2646 Fairmont Blvd. Cleveland, OH 44106 Email: [email protected]

Broughan, Thomas A., MD INACTIVE | 2011 Inova Fairfax Hospital Email: [email protected]

Brousert, Peter RESIDENT | 2013 Institute of Pathology Address: Breisachesstrasse 115a Freiburg, 79106 Germany Email: [email protected]

Broussard, Brett, MD RESIDENT | 2013 Univ. of Alabama at Birmingham Address: 3509 Woodruff Circle Birmingham, AL 35216 Email: [email protected]

Browder, William, MD INACTIVE | 2009 East Tennessee State Univ. Email: [email protected]

Brown, Erin, MD INACTIVE | 2011 UC Davis Email: [email protected]

Brown, Kimberly, MD ACTIVE | 2014 Univ. of Texas Medical Branch Address: 301 Univ. Blvd. Galveston, TX 77555-0541 Email: [email protected]

Brunicardi, F. Charles, MD INACTIVE | 2010 Methodist Hospital Email: [email protected]

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Bruno, Morgan L. MS ACTIVE | 2014 M.D. Anderson Cancer Center Surgical Oncology Address: 1515 Holcombe Blvd. Houston, TX 77030 Email: [email protected]

Buchler, Markus W., MD INACTIVE | 2009 Univ. of Heidelberg Email: [email protected]

Burke, Erin, MD RESIDENT | 2014 Univ. of Minnesota Dept. of Surgery Address: 420 Delaware St. SE MMC 195 Minneapolis, MN 55455 Email: [email protected]

Burkhart, Richard, MD RESIDENT | 2013 Thomas Jefferson Univ. Hospital Address: 1015 Walnut St., Suite 611A Philadelphia, PA 19107 Email: [email protected]

Butler, James, MD RESIDENT | 2014 Indiana Univ. Address: Emerson Hall - Room 202 545 Barnhill Dr. Indianapolis, IN 46202 Email: [email protected]

Butte, Jean, MD RESIDENT | 2014 Univ. of Calgary Address: 716 34th St., Basement Calgary, AB T2N 2Y2 Canada

Byrd, David R., MD INACTIVE | 2009 Univ. of Washington Email: [email protected]

Callery, Mark, MD INACTIVE | 2012 Beth Israel Deaconess Medical Center Email: [email protected]

Cameron, John L., MD ACTIVE | 2013 Johns Hopkins Hospital Address: 1800 Orleans St., Blalock 679 Baltimore, MD 21287 Email: [email protected]

Cappelli, Carla, MD, PhD ACTIVE | 2013 Univ. of Pisa Diagnostic and Interventional Radiology Address: via Paradisa 2 Pisa, 56126 Italy Email: [email protected]

Cardona, Kenneth, MD INACTIVE | 2012 Emory Univ. School of Medicine Email: [email protected]

Carroll, Jr., James E., MD INACTIVE | 2010 Univ. of Massachussetts Medical School Email: [email protected]

Carter, Ross, MD ACTIVE | 2013 Glasgow Royal Infirmary West of Scotland Pancreatic Unit Glasgow, G61 3BB UK Email: [email protected]

Carter, Timothy INACTIVE | 2012 Email: [email protected]

Cascini, Francesco Paulo INACTIVE | 2011 Bio-Medico Campus, Univ. of Rome Email: [email protected]

Casey Bounds, Brenna, MD INACTIVE | 2011 Massachusetts General Hospital Email: [email protected]

Castellanos, Jason, MD RESIDENT | 2014 Vanderbilt Univ. Medical Center Address: 4040 Woodlawn Dr. #12 Nashville, TN 37205 Email: [email protected]




Castello, Juliana, MD INACTIVE | 2010 MD Anderson Cancer Center Email: [email protected]

Cattaruzza, Fiore INACTIVE | 2012 Email: [email protected]

Cauley, Christy, BS INACTIVE | 2011 Indiana Univ. School of Medicine Email: [email protected]

Ceppa, Eugene, MD ACTIVE | 2013 Indiana Univ. School of Medicine Address: 545 Barnhill Dr, EH 517 Indianapolis, IN 46202 Email: [email protected]

Cha, Charles, MD INACTIVE | 2009 Yale Univ. School of Medicine Email: [email protected]

Chabot, John, MD ACTIVE | 2014 Columbia Univ. Medical Center Address: 161 Fort Washington Ave. New York, NY 10032 Email: [email protected]

Chan, Carlos, MD ACTIVE | 2014 National Institute of Medical Sciences General Surgery Address: Vasco de Quiroga 15, Tlalpan Mexico, D.F. 15000 Mexico Email: [email protected]

Charnley, Richard M DM, FRCS ACTIVE | 2014 Newcastle upon Tyne Hospitals Surgery Address: Freeman Hospital, Freeman Rd. High Heaton Newcastle upon Tyne, NE7 7DN UK Email: [email protected]

Chatterjee, Deyali, MD INACTIVE | 2011 MD Anderson Cancer Center Email: [email protected]

Chau, Zeling RESIDENT | 2013 Beth Israel Deaconess Medical Ctr. Address: 330 Brookline Ave. Boston, MA 02115 Email: [email protected]

Chauhan, Shailendra, MD INACTIVE | 2009 Univ. of S. Florida Email: [email protected]

Chen, Kathryn, MD RESIDENT | 2013 Fox Chase Cancer Center Address: 333 Cottman Ave. Philadelphia, PA 19111 Email: [email protected]

Cherenfant, Jovenel, MD ACTIVE | 2014 Franciscan Hammond Clinic Surgery Address: 9800 Valparaiso Dr. Munster, IN 46321 Email: [email protected]

Cho, Clifford S., MD ACTIVE | 2014 Univ. of Wisconsin School of Medicine Dept. of Surgery Address: J4/703 CSC, 600 Highland Ave. Madison, WI 53792 Email: [email protected]

Chopin-Laly, Xavier, MD INACTIVE | 2010 MD Anderson Cancer Center Email: [email protected]

Choti, Michael, MD, MBA ACTIVE | 2014 UT Southwestern Med Center Dept. of Surgery Address: 5323 Harry Hines Blvd. Dallas, TX 75390-9031 Email: [email protected]

Choung, Edward INACTIVE | 2012 Email: [email protected]

115



Christein, John, MD ACTIVE | 2014 Univ. of Alabama at Birmingham Dept. of Surgery Address: 1720 2nd Ave. S, KB429 Birmingham, AL 35294-0016 Email: [email protected]

Christians, Kathleen, MD ACTIVE | 2014 Medical College of Wisconsin Surgical Oncology Address: 9200 W. Wisconsin Ave. Milwaukee, WI 53214 Email: [email protected]

Chugh, Rohit, MD RESIDENT | 2013 Univ. of Minnesota Address: 420 Deleware St. SE Minneapolis, MN Email: [email protected]

Chun, Yun Shin, MD INACTIVE | 2011 Fox Chase Cancer Center Email: [email protected]

Ciuffreda, Mauro INACTIVE | 2012 Email: [email protected]

Clain, Jonathan, MD INACTIVE | 2011 Mayo Clinic Email: [email protected]

Clancy, Thomas, MD ACTIVE | 2014 Brigham & Women’s Hospital/Harvard Medical School Dept. of Surgery Address: 75 Frances St. Boston, MA 02043 Email: [email protected]

Clark, Clancy, MD ACTIVE | 2014 Wake Forrest Baptist Health General Surgery-Surgical Oncology Address: Medical Center Blvd. Winston Salem, NC 27157 Email: [email protected]

Clark, Whalen, MD RESIDENT | 2013 Univ. of South Florida Dept. of Surgery Address: 1001 S. Rome Ave., #2 Tampa, FL 33606 Email: [email protected]

Clegg, Carol MS INACTIVE | 2011 MD Anderson Cancer Center Email: [email protected]

Coelho, Ana Maria, MD, PhD RESIDENT | 2013 Univ. of Sao Paulo Address: R Joao Moura 690 #41 Sao Paulo, SP 5412001 Brazil Email: [email protected]

Coelho, Nelson Vieira, MD ACTIVE | 2013 Fundacao de Gastroenterologia Endoscopy Address: Silva So 255, Porto Alegre, 90610-270 Brazil Email: [email protected]

Contreras, Carlo, MD INACTIVE | 2010 MD Anderson Cancer Center Email: [email protected]

Conway, W. Charles, MD ACTIVE | 2014 Ochsner Medical Center Surgery Address: 1514 Jefferson Hwy., CT-8 New Orleans, LA 70121 Email: [email protected]

Cooper, Amanda, MD RESIDENT | 2014 MD Anderson Cancer Center Dept. of Surgical Oncgology Address: 1400 Pressler St. Unit 1484 Houston, TX 77030 Email: [email protected]

Cooper, Michol, MD, PhD RESIDENT | 2013 Johns Hopkins Hospital Address: 600 N. Wolfe St., Halsted 610 Baltimore, MD 21287 Email: [email protected]




Coppola, Roberto, MD ACTIVE | 2014 Univ. Campus Bio-Medico - Rome General Surgery Address: Via Alvaro del Portillo 200 Rome, 00128 Italy Email: [email protected]

Coppola, Alessandro RESIDENT | 2014 Catholic Univ. of Sacred Heart Address: largo A. Gemelli, 1 Rome, 00100 Italy Email: [email protected]

Correa, Camilo, MD INACTIVE | 2009 Mass General Hospital Email: [email protected]

Crippa, Stefano, MD INACTIVE | 2011 Policlinico GB Rossi Verona Email: [email protected]

Cui, Yunfeng, MD INACTIVE | 2010 Johns Hopkins Bayview Medical Center Email: [email protected]

Cullen, Joseph J., MD ACTIVE | 2014 Univ. of Iowa Hospitals and Clinics Dept. of Surgery Address: 200 Hawkins Drive, 1528 JCP Iowa City, IA 52242 Email: [email protected]

Cunha, Jose Eduardo, MD ACTIVE | 2013 Sao Paulo Univ. Medical School Associate Professor of Surgery Address: Rua Oquira 116 Sao Paulo, SP 5467030 Brazil Email: [email protected]

Cunningham, Steven, MD ACTIVE | 2013 Saint Agnes Hospital Address: 900 Caton Ave. Baltimore, MD 21229 Email: [email protected]

Dale, Jonas, MD INACTIVE | 2010 Haukeland Univ. Hospital Email: [email protected]

Daouadi, Mustapha INACTIVE | 2012 Email: [email protected]

Datta, Jashodeep, MD RESIDENT | 2014 Univ. of Pennsylvania Address: 3400 Spruce St. Philadelphia, PA 19129 Email: [email protected]

De Campos, Tercio, MD INACTIVE | 2012 Santa Casa School of Medicine Email: [email protected]

De Jesus-Monge, Wilfredo, MD, MSc INACTIVE | 2011 Univ. of Massachusetts Medical School Email: [email protected]

de la Fuente, Sebastian, MD ACTIVE | 2013 Florida Hospital Orlando and Univ. Central Florida Address: 2415 N. Ornage Ave., Suite 400 Orlando, FL 32804 Email: [email protected]

Del Chiaro, Marco, MD, PhD ACTIVE | 2014 Karolinska Instutitet Address: Division of Surgery K53 Karolinska Univ. Hospital Huddinge Stockholm, 14186 Sweden Email: [email protected]

Delitto, Daniel, MD RESIDENT | 2014 Univ. of Florida Address: 5011 NW 1st Pl. Gainesville, FL 32607 Email: [email protected]

Demeure, Michael J., MD, MBA ACTIVE | 2014 Translational Genomics Research Institute Integrated Cancer Genomics Address: 9475 E Ironwood Square, Suite 102 Scottsdale, AZ 85258 Email: [email protected]

117



Demirjian, Aram N., MD ACTIVE | 2014 Univ. of California-Irvine Hepatobiliary and Pancreas Surgery Address: 333 City Boulevard West, Suite 1205 Orange, CA 92868 Email: [email protected]

Denbo, Jason, MD INACTIVE | 2011 Univ. of Tennessee Health Science Center Email: [email protected]

Desai, Rajendra, MS, DNB, MCh, FRCS ACTIVE | 2014 Kamineni Hospital Ltd HPB Surgery and Liver Transplantation Address: 3-6-261, Himayatnagar, Flat 303, 3rd Floor, Tirumala Apartments Hyderabad, 500029 India Email: [email protected]

Desaki, Ryosuke RESIDENT | 2014 Email: [email protected]

Deziel, Daniel, MD INACTIVE | 2010 Univ. Surgeons Email: [email protected]

Dholakia, Avani, BS RESIDENT | 2013 Johns Hopkins Univ. School of Medicine Address: 401 N. Broadway Baltimore, MD 21231 Email: [email protected]

DiNorcia, Joe INACTIVE | 2012 Email: [email protected]

Distler, Marius, MD RESIDENT | 2013 Univ. of Dresden Address: Fetscher Str. 74 Dresden, 01307 Germany Email: [email protected]

Dixon, Elijah, MD ACTIVE | 2014 Univ. of Calgary Dept. of Surgery & Oncology Address: 108 Solace Ridge Place Calgary, AB T3Z 3M9 Canada Email: [email protected]

Dominguez, Ismael, MD INACTIVE | 2009 Institute Nacional de Medicine Email: [email protected]

Donahue, Timothy, MD ACTIVE | 2014 UCLA David Geffen School of Medicine Surgery Address: 10833 Le Conte Ave., 72-256 CHS Los Angeles, CA 90095-6904 Email: [email protected]

Downs-Canner, Stephanie, MD RESIDENT | 2014 Univ. of Pittsburgh Medical Center Address: 200 Lothrop St., Room 679 PUH Pittsburgh, PA 15213 Email: [email protected]

Dudeja, Vikas, MD RESIDENT | 2014 Memorial Sloan-Kettering Cancer Center Address: Program1275 York Ave. New York, NY 10065 Email: [email protected]

Duff, Michelle, DPT INACTIVE | 2010 Pancreatic Cancer Action Network (PanCAN) Email: [email protected]

Duncan, Casey, MD RESIDENT | 2013 Univ. of Texas Medcal Branch Address: 301 Univ. Blvd. Galveston, TX 77555-0534 Email: [email protected]

Duncan, Mark, MD INACTIVE | 2009 Johns Hopkins Bayview Email: [email protected]

Duque, Marvin, MD RESIDENT | 2013 Tufts Medical Center Address: 800 Washington St., #245 Boston, MA 02111 Email: [email protected]




Duxbury, Mark, MA, DM, FRCSEd ACTIVE | 2013 Glasgow Royal Infirmary Address: Alexandra Parade Glasgow, G31 2ER UK Email: [email protected]

Dwinell, Michael, PhD INACTIVE | 2011 Medical College of Wisconsin Email: [email protected]

Edil, Barish, MD ACTIVE | 2014 University of Colorado Hospital Address: 1665 Aurora Court, Rm. 3337, MS F-703 Aurora, CO 80045 Email: [email protected]

Egawa, Shinichi, MD INACTIVE | 2009 Tohoku Univ. Email: [email protected]

Eibl, Guido, MD INACTIVE | 2009 David Geffen School of Medicine at UCLA Email: [email protected]

Einersen, Peter, BA RESIDENT | 2013 Columbia Univ. Medical Center Address: 161 Ft. Washington Ave. New York, NY 10032 Email: [email protected]

El-Hayek, Kevin M., MD ACTIVE | 2014 Cleveland Clinic General Surgery Address: 9500 Euclid Ave. Cleveland, OH 44195 Email: [email protected]

Ellison, Trevor, MD INACTIVE | 2010 Johns Hopkins Medical Center Email: [email protected]

Engebretson, Anitra, BS ACTIVE | 2014 Pancreatic Cancer Action Network (PanCAN) Patient Services Address: 1500 Rosecrans Ave., Suite 200 Manhattan Beach, CA 90260 Email: [email protected]

Epelboym, Irene, MD RESIDENT | 2013 Columbia Univ. Medical Center Surgery; Pancreas Center Address: 161 Fort Washington Ave., 8th Fl. New York, NY 10032 Email: [email protected]

Erdmann, Joris, MD RESIDENT | 2013 Erasmus MC Rotterdam, Netherlands Email: [email protected]

Evans, Douglas B., MD ACTIVE | 2014 Medical College of Wisconsin Dept. of Surgery Address: 9200 W. Wisconsin Ave., Suite 3510 Milwaukee, WI 53226 Email: [email protected]

Evans, Anna, MD RESIDENT | 2014 Yale New Haven Hospital Address: 313 Mansfield St., Apt 2 New Haven, CT 06511 Email: [email protected]

Falconi, Massimo, MD ACTIVE | 2014 Universiti Politecnica dlel Marche Clinica Chirurgia del pancreas Address: Ospedali Riuniti, Via Conca 71 Ancona-Torrette, 60126 Italy Email: [email protected]

Fan, Katherine RESIDENT | 2013 Email: [email protected]

Farkas, Jr., Gyula Andras, MD, PhD ACTIVE | 2014 Univ. of Szeged Surgery Address: Szokefalvi-Nagy Gyula u.6 Szeged, 06720 Hungary Email: [email protected]

Farnell, Michael B., MD ACTIVE | 2014 Mayo Clinic Dept. of Surgery Address: 200 First St. NW Rochester, MN 55905 Email: [email protected]

119



Farrell, James, MD ACTIVE | 2014 Yale Univ. Address: 333 Cedar St. New Haven, CT 06520 Email: [email protected]

Fatima, Javairiah, MD INACTIVE | 2009 Mayo Clinic College of Medicine Email: [email protected]

Feng, Zizhen, MD, PhD RESIDENT | 2013 Email: [email protected]

Fergusson, James, MD INACTIVE | 2011 The Canberra Hospital Email: [email protected]

Fernandez-Cruz, Laureano, MD, FRCS(Ed) INACTIVE | 2011 Univ. of Barcelona Email: [email protected]

Fernandez-del Castillo, Carlos, MD ACTIVE | 2014 Massachusetts General Hospital Surgery Address: 15 Parkman St., ACC 460 Boston, MA 02114 Email: [email protected]

Ferrara, Michael, MS INACTIVE | 2012 Mayo Clinic Email: [email protected]

Ferrone, Cristina, MD ACTIVE | 2014 Mass Gen Hospital Address: 15 Parkman St., Wang 460 Boston, MA 02108 Email: [email protected]

Fischer, Craig, MD INACTIVE | 2012 The Methodist Hospital Email: [email protected]

Fisher, Alex, MS RESIDENT | 2014 Address: 3526 Pape Ave., #2 Cincinnati, OH 45208 Email: [email protected]

Fisher, William E., MD ACTIVE | 2014 Baylor College of Medicine Address: 6620 Main St., Suite 1450 Houston, TX 77030 Email: [email protected]

Fleming, Jason B., MD ACTIVE | 2014 Univ. of Texas, MD Anderson Cancer Center Division of Surgical Oncology Address: 1400 Pressler St., Unit 1484, PO Box 301402 Houston, TX 77030-1402 Email: [email protected]

Flint, Gregg, BS RESIDENT | 2013 Address: 1304 West Targee St. Boise, ID 83706 Email: [email protected]

Fong, Zhi Ven, MD RESIDENT | 2014 Massachusetts General Hospital Surgery Address: 55 Fruit St., GRB 425 Boston, MA 02114 Email: [email protected]

Franco, Jan, MD, PhD ACTIVE | 2014 Mercy Medical Ctr - DSM Address: 411 Laurel St., Des Moines, IA 50314 Email: [email protected]

Frederick, Wayne A. I., MD INACTIVE | 2010 Howard Univ. Email: [email protected]

Frey, Charles, MD INACTIVE | 2012 Email: [email protected]

Fronza, Jeffrey, MD INACTIVE | 2009 Northwestern Univ. School of Medicine Email: [email protected]

Fuchshuber, Pascal, MD, PhD INACTIVE | 2012 The Permanente Medical Group, Inc. Walnut Creek Medical Ctr. Email: [email protected]




Fujimoto, Jiro, MD, PhD ACTIVE | 2014 Hyogo College of Medicine Dept. of Surgery Address: 1-1 Mukogawa-cho Nishinomiya, Hyogo 663-8501 Japan Email: [email protected]

Fujinaga, Kazuhisa RESIDENT | 2014 Japan Email: [email protected]

Funel, NIccola, PhD ACTIVE | 2013 Dept. of Translational Research on New Technologies Address: via paradisa, 2 pisa, 56124 Italy Email: [email protected]

Gamarra, Roberto, MD INACTIVE | 2011 William Beaumont Hospital Email: [email protected]

Ganai, Sabha, MD, PhD ACTIVE | 2014 Southern Illinois Univ. Address: Simmons Cancer Institute, 315 W Carpenter St. Springfield, IL 62702 Email: [email protected]

Gao, Qingshen, MD ACTIVE | 2013 NorthShore Univ. HealthSystem Address: 1001 Univ. Place Evanston, IL 60201 Email: [email protected]

Gareer, Haytham, MD RESIDENT | 2014 National Cancer Institute, Cairo Univeristy Address: Fom El Khaleg Cairo, Egypt Email: [email protected]

Gaujoux, Sebastien, MD INACTIVE | 2013 AP-HP Hôpital Beaujon Email: [email protected]

Gauvin, Jeffrey, MD INACTIVE | 2011 UC Davis Email: [email protected]

Gawlas, Irmina, BA RESIDENT | 2013 Columbia Univ. Medical Center Address: 161 Fort Washington Ave. New York, NY 10032 Email: [email protected]

Gecelter, Gary, MD INACTIVE | 2012 Email: [email protected]

Gelrud, Andres, MD INACTIVE | 2009 Univ. of Pittsburgh Email: [email protected]

Gilbert, Erin, MD ACTIVE | 2014 Oregon Health & Science Univ. General Surgery Address: 3181 SW Sam Jackson Park Rd., L223A Portland, OR 97239 Email: [email protected]

Giovannetti, Elisa, MD, PhD ACTIVE | 2014 Univ. of Pisa Address: Via Roma 55 Pisa, 56100 Italy Email: [email protected]

Girelli, Roberto, MD INACTIVE | 2010 Casa Di Cura Dott. Pederzoli Email: [email protected]

Glasgow, Robert, MD INACTIVE | 2011 Univ. of Utah Email: [email protected]

Go, Vay Liang, MD ACTIVE | 2014 UCLA Digestive Diseases Address: 900 Veteran Ave, Warren Hall 13-146 Los Angeles, CA 90095 Email: [email protected]

Godoy, Renato, MD INACTIVE | 2011 Faculdade de Medicina USP Email: [email protected]

121



Goldberg, Ross, MD INACTIVE | 2010 Thomas Jefferson Univ. Hospital Email: [email protected]

Golkar, Farhaad, MD INACTIVE | 2011 Tampa General Hospital Email: [email protected]

Goni, Elisabetta, MD RESIDENT | 2013 San Raffaele Scientific Institute Gastroenterology Address: Via Olgettina 58 Milan, 20132 Italy Email: [email protected]

Gonzalez, Carlos, MD RESIDENT | 2013 Indiana Univ. School of Medicine Address: 13829 Black Canyon CT Fishers, IN 46038 Email: [email protected]

Gooszen, Hein, MD INACTIVE | 2010 UMC Utrecht Email: [email protected]

Goyal, Kush, MD INACTIVE | 2009 Univ. Hospitals Case Medical Center Email: [email protected]

Grady, Eileen F., PhD INACTIVE | 2011 UCSF Email: [email protected]

Greenblatt, David Yu, MD, MSPH INACTIVE | 2011 Univ. of Wisconsin Email: [email protected]

Grignol, Valene INACTIVE | 2009 Email: [email protected]

Gruetzmann, Robert, MD ACTIVE | 2013 Dresden Univ. Germany Email: [email protected]

Grundfest-Broniatowski, Sharon, MD INACTIVE | 2009 Cleveland Clinic A80 Email: [email protected]

Guglielmo, Nicola, MD RESIDENT | 2013 Sapienza Paride Stefanini Address: Via Genzano 87 Rome, 00179 Italy Email: [email protected]

Gupta, Rajesh MBBS, MS, M Ch ACTIVE | 2014 PGIMER Surgical Gastroenterology Div., Dept. of General Surgery Address: Sector 12 Chandigarh, 160012 India Email: [email protected]

Gusani, Naraj, MD INACTIVE | 2009 Penn State Hershey Medical Center Email: [email protected]

Gust, Shannon INACTIVE | 2009 Johns Hopkins Hospital Email: [email protected]

Guzzetta, Angela INACTIVE | 2012 Email: [email protected]

Gvozdenović, Miomir S., MD ACTIVE | 2013 Clinical Center of Serbia Emergency Center Address: Pasterova 8 Belgrade, 11000 Serbia Email: [email protected]

Haglund, Ulf, MD INACTIVE | 2009 Uppsala Univ. Hospital Email: [email protected]

Hamilton, Nicholas, MD INACTIVE | 2009 Washington Univ. Email: [email protected]

Hao, Disi INACTIVE | 2012 Email: [email protected]




Hardacre, Jeffrey, MD ACTIVE | 2014 Univ. Hospitals Case Medical Ctr. Dept of Surgery Address: 11100 Euclid Ave. Cleveland, OH 44106 Email: [email protected]

Hari, Danielle, MD INACTIVE | 2009 NIH Email: [email protected]

Harper, Megan, BS INACTIVE | 2012 UC San Diego Moores Cancer Center Email: [email protected]

Hashimoto, Yasushi, MD RESIDENT | 2013 Hiroshima Univ. Hospital Address: 1-2-3 Kasumi, Minami-ku Hiroshima, 734-8551 Japan Email: [email protected]

Hassanain, Ehab, MD INACTIVE | 2009 SUNY Downstate Medical Center Email: [email protected]

Hatcher, Thomas S., MD INACTIVE | 2011 Univ. of Mississippi Medical Center Email: [email protected]

Hawkins, William G., MD ACTIVE | 2014 Washington Univ. School of Medicine Dept. of Surgery Address: 660 S. Euclid Ave., Campus Box 8109 St. Louis, MO 63110 Email: [email protected]

He, Jin, MD, PhD INACTIVE | 2011 Johns Hopkins Hospital Email: [email protected]

Helling, Thomas S., MD INACTIVE | 2010 Univ. of Mississippi Medical Center Email: [email protected]

Heneghan, Rachel, MD RESIDENT | 2013 Virginia Mason Medical Center Address: 1100 9th Ave., H8-GME Seattle, WA 98101 Email: [email protected]

Hermeneit, Sonja, MD INACTIVE | 2009 Universit Rastock Email: [email protected]

Hernandez, Jonathan, MD INACTIVE | 2011 USF Email: [email protected]

Herrera-Caceres, Jaime O., MD RESIDENT | 2013 Address: Moctezuma 56 interior 3 Ciudad de Mexico, 14050 Mexico Email: [email protected]

Hewitt, Kelly, MD RESIDENT | 2013 Univ. of Utah Address: 1950 Circle of Hope, Ste. HCH N-6405 Salt Lake City, UT 84132 Email: [email protected]

Heywood, Glenroy, MD INACTIVE | 2011 Email: [email protected]

Hill, Joshua, MD INACTIVE | 2009 Univ. of Massachusetts Email: [email protected]

Hines, Joe, MD INACTIVE | 2012 UCLA School of Medicine Email: [email protected]

Hirono, Seiko, MD ACTIVE | 2014 Wakayama Medical Univ. Second Dept. of Surgery Address: 811-1 Kimiidera, Wakayama, 641-8510 Japan Email: [email protected]

Hirose, Kenzo, MD INACTIVE | 2010 Johns Hopkins Univ. Email: [email protected]

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Hodul, Pamela, MD ACTIVE | 2014 H. Lee Moffitt Cancer Center & Research Institute Dept. of Gastrointestinal Oncology Address: 12902 Magnolia Drive, FOB-2 Tampa, FL 33612 Email: [email protected]

Hoffman, John P., MD ACTIVE | 2014 Fox Chase Cancer Center Surgery Address: 333 Cottman Ave. Philadelphia, PA 19111 Email: [email protected]

Hogg, Melissa, MD ACTIVE | 2014 Univ. of Pittsburgh Medical Center Pittsburgh, PA Email: [email protected]

Holbrook, Ryan, MD INACTIVE | 2010 Cancer Care Northwest Email: [email protected]

Honselmann, Kim, MD RESIDENT | 2014 Univ. Medical Center Schleswig-Holstein, Campus Luebeck Address: Ratzeburgerallee 160 Luebeck, 23538 Germany Email: [email protected]

Hopt, Ulrich T., MD ACTIVE | 2014 Univ. of Freiburg Surgery Address: Hugstetter Str. 55, Freiburg, D 75106 Germany Email: [email protected]

Hornick, John, MD INACTIVE | 2010 Washington Univ. School of Medicine Email: [email protected]

Horvath, Karen, MD INACTIVE | 2011 Univ. of Washington Email: [email protected]

Hotz, Hubert, MD INACTIVE | 2009 Charite School of Medicine Campus Ben Franklin Email: [email protected]

House, Michael, MD ACTIVE | 2014 Indiana Univ. School of Medicine Address: 545 Barnhill Drive, EH 529 Indianapolis, IN 46202 Email: [email protected]

Howard, Thomas, MD INACTIVE | 2012 Indiana Univ. Medical Center Email: [email protected]

Hruban, Ralph H., MD ACTIVE | 2014 John Hopkins Univ. SOM Pathology Address: 401 N. Broadway, Weinberg 2242 Baltimore, MD 21231 Email: [email protected]

Huang, Qi INACTIVE | 2012 Email: [email protected]

Hughes, Steven J., MD ACTIVE | 2014 Uf Health Shands General Surgery Address: 1600 SW Archer Rd., Po Box 100109 Gainesville, FL 32610 Email: [email protected]

Hurtuk, Michael INACTIVE | 2012 Email: [email protected]

Huss, Harold T., DO ACTIVE | 2014 CTCA Illinois Surgical Onology Address: 2520 Elisha Ave. Zion, IL 60203 Email: [email protected]




Hwang, Rosa F., MD ACTIVE | 2014 UT – MD Anderson Cancer Center Surgical Oncology Address: PO Box 301402, Unit 1484 Houston, TX 77230-1402 Email: [email protected]

Iacobuzio, Christine, MD, PhD INACTIVE | 2009 Johns Hopkins Medical Institution Email: [email protected]

Ideno, Noboru, MD ACTIVE | 2013 Kyushu Univ. Dept. Surgery and Oncology Address: 3-1-1 Maidashi, Higashi-ku Fukuoka, 812-8582 Japan Email: [email protected]

Isaji, Shuji, Prof. ACTIVE | 2014 Mie Univ. Graduate School of Medicine Hepatobiliary Pancreatic and Transplant Surgery Address: 2-174, Edobashi Tsu, Mie 514-8507 Japan Email: [email protected]

Ito, Hiromichi, MD, FACS ACTIVE | 2014 Michigan State Univ. Dept. of Surgery Address: 1200 E Michigan Ave., Suite 655 East Lansing, MI 48823 Email: [email protected]

Jackson, Patrick G., MD INACTIVE | 2009 Georgetown Univ. Medical Center Email: [email protected]

Jacobs, Michael J., MD ACTIVE | 2014 St John Providence Hospital Surgery Address: 820 Puritan Ave. Birmingham, MI 48009 Email: [email protected]

Jamieson, Nigel, MRCS, PhD RESIDENT | 2013 West of Scotland Pancreatic Unit Address: Glasgow Royal Infirmary, Glasgow, Lanarkshire G31 2ER UK Email: [email protected]

Jang, Jin-Young, MD, PhD ACTIVE | 2014 Seoul Nat’l Univ. Hosptial Dept. of Surgery Address: Yongon-dong 28, Chongno-gu Seoul, Korea Email: [email protected]

Jensen, Eric H., MD ACTIVE | 2014 Univ. of Minnesota Surgical Oncology Address: 420 Delawaare St. SE, MC195 Minneapolis, MN 55455 Email: [email protected]

Joehl, Raymond J., MD RETIRED/HONORARY | 2014 Hines VA Hospital Surgical Service (112) Address: 5th Ave. & Roosevelt Rd. Hines, IL 60141 Email: [email protected]

Johnson, Mike, MD INACTIVE | 2009 Cleveland Clinic Email: [email protected]

Johnston, Cory, MD INACTIVE | 2011 Univ. of Utah Email: [email protected]

Juhani, Sand, MD, PhD ACTIVE | 2013 Tampere Univ. Hospital Address: Tersbondie 35, Tampere, 33521 Finland Email: [email protected]

Jukemura, José, MD INACTIVE | 2012 Univ. of Sao Paulo Email: [email protected]

125



Jury, Robert P., MD ACTIVE | 2014 Royal Oak Surgical Associates Address: 3535 W. 13 Mile Rd. #205 Royal Oak, MI 48073 Email: [email protected]

Kadera, Brian, MD RESIDENT | 2013 Univ. of California - Los Angeles Surgery Address: 10833 LeConte Ave, 72-235 CHS Los Angeles, CA 90095 Email: [email protected]

Kalish, Brian INACTIVE | 2012 Email: [email protected]

Kato, Hiroyuki, MD INACTIVE | 2011 Mie Graduate School of Medicine Email: [email protected]

Katz, Matthew, MD ACTIVE | 2014 MD Anderson Cancer Center Surgical Oncology Address: 1400 Pressler St., Unit 1484 Houston, TX 77030 Email: [email protected]

Kavuturu, Srinivas, MD INACTIVE | 2011 Milton S Hershey Medical Center & College of Medicine Email: [email protected]

Kawaguchi, Kei, MD, PhD ACTIVE | 2014 Tohoku Univ. Graduate School of Medicine Address: 1-1, Seiryo-machi, Aoba-ku Sendai, Miyagi 980-8574 Japan Email: [email protected]

Kawai, Manabu, MD, PhD ACTIVE | 2014 Wakayama Medical Univ. Second Dept. of Surgery Address: Kimiidera 811-1 Wakayama, 641-8510 Japan Email: [email protected]

Kazantsev, George, MD ACTIVE | 2014 Kaiser Foundation Hospital Surgery Address: 3600 Broadway, Third Floor Oakland, CA 94611 Email: [email protected]

Keck, Tobias, MD ACTIVE | 2014 Univ. Hospital of Schleswig Holstein, Campus Lübeck Dept. of Surgery Address: Ratzeburger Allee 160 Lüebeck, 23568 Germany Email: [email protected]

Keim, Rebecca, MD ACTIVE | 2014 St. Peter’s Health Partners Medical Associates General Surgery Address: 319 S. Manning Blvd., Suite 305 Albany, NY 12208 Email: [email protected]

Keith, Roger G., MD INACTIVE | 2010 Royal Univ. Hospital Email: [email protected]

Kelly, Kaitlyn INACTIVE | 2012 Email: [email protected]

Kelly, Tracy, MD INACTIVE | 2011 Medical College of Wisconsin Email: [email protected]

Kendrick, Michael, MD ACTIVE | 2014 Mayo Clinic Divison of GI and General Surgery Address: 200 First St., SW Rochester, MN 55905 Email: [email protected]

Kennedy, Eugene, MD ACTIVE | 2013 Address: 80 Horseshoe Pt. Phoenixville, PA 19460 Email: [email protected]




Kent, Tara, MD ACTIVE | 2013 Beth Israel Deaconess Medical Center Dept. Surgery Address: 330 Brooklyn Ave. Suite 9 Boston, MA 02115 Email: [email protected]

Khan, Saboor, MBBS, PhD INACTIVE | 2010 Mayo Clinic Email: [email protected]

Kim, Michael, MD INACTIVE | 2011 MD Anderson Cancer Center Email: [email protected]

King, Jonathan INACTIVE | 2012 Email: [email protected]

Kirkwood, Kimberly S., MD ACTIVE | 2014 Univ. of California - San Francisco General Surgery Address: 521 Parnassus Ave. Room C-341, Box 0790 San Francisco, CA 94143 Email: [email protected]

Kishiwada, Masashi, MD, PhD ACTIVE | 2014 Mie Univ. Address: yumegaoka, Tsu Mie, 514-0116 Japan Email: [email protected]

Kiswani, Vandhana INACTIVE | 2012 Email: [email protected]

Kitagawa, Hirohisa, MD ACTIVE | 2014 Kanazawa Univ. Address: 13-1 Takaramachi, Kanazawa, 920-8641 Japan Email: [email protected]

Kitagawa, Yuichi, MD ACTIVE | 2014 National Center for Geriatrics & Gerontology Dept. of Surgery Address: 35 Morioka Gengo, Obu, Japan Email: [email protected]

Klar, Ernst, MD ACTIVE | 2014 Univ. of Rostock Dept. of Surgery Address: Chirurgische Klinik und Poliklinik Schillingallee 35 Rostock, 18057 Germany Email: [email protected]

Kleiner, Daniel, MD RESIDENT | 2013 Washington Univ. in St. Louis Address: 2454 Ivy Springs Lane, Charlottesville, VA 22901 Email: [email protected]

Kline, Jessica M., BS INACTIVE | 2009 Thomas Jefferson Univ. Email: [email protected]

Kluger, Michael D., MD, MPH ACTIVE | 2014 Columbia College of Physicians and Surgeons Surgery Address: 161 Fort Washington Ave., 8th Floor New York, NY 10032 Email: [email protected]

Koay, Eugene, MD, PhD RESIDENT | 2013 MD Anderson Cancer Center Address: 1220 Holcombe, MS 97 Houston, TX 77030 Email: [email protected]

Kobayashi, Hironori, MD INACTIVE | 2012 Hiroshima Univ. Email: [email protected]

Kobayashi, Motoyuki INACTIVE | 2012 Email: [email protected]

Kok, Niels, MD, PhD ACTIVE | 2013 Erasmus MC Address: PO Box 2040, Rotterdam, 3000 CA Netherlands Email: [email protected]

127



Kolarczyk, Aleksandra, Ms RESIDENT | 2013 Medical Univ. of Silesia, Katowice Poland Address: Jastrzebia 8/3, Sosnowiec, - 41-209 Poland Email: [email protected]

Kondo, Naru, MD RESIDENT | 2014 Hiroshima Univ. Dept. of Surgery Address: Kasumi, Minami-Ku Hiroshima, 7328551 Japan Email: [email protected]

Kondo, Yuichi, MD, PhD INACTIVE | 2011 Hyogo College of Medicine Email: [email protected]

Konstantinidis, Ioannis, MD INACTIVE | 2010 Mass General Hospital Email: [email protected]

Korotkov, Sergey RESIDENT | 2013 9th Minsk Municipal Hospital emergency abdominal surgery Address: Semashko 8 Minsk, 220116 Belarus Email: [email protected]

Kosaka, Hisashi, MD, PhD ACTIVE | 2014 Hyogo College of Medicine Surgery Address: 1-1 Mukogawa-tyou Nishinomiya, Hyogo 663-8501 Japan Email: [email protected]

Krantz, Seth, MD INACTIVE | 2011 Northwestern Univ. Email: [email protected]

Krepline, Ashley RESIDENT | 2014 Medical College of Wisconsin Milwaukee, WI 53226 Email: [email protected]

Kubat, Eric, MD INACTIVE | 2011 Univ. of California, San Francisco Email: [email protected]

Kuehn, Florian, MD RESIDENT | 2014 Univ. of Rostock Address: Schillingallee 35 Rostock, 18057 Email: [email protected]

Kuroda, Nobukazu, MD, PhD ACTIVE | 2013 Hyogo College of Medicine Dept. of Surgery Address: 1-1, Mukogawa-cho, Nishinomiya, Hyogo 6638501 Japan Email: [email protected]

Kusnierz, Katarzyna, MD, PhD ACTIVE | 2013 Medical Univ. of Silesia Dept. of Gastroenterology Address: Medykow 14 Katowice, 40-752 Poland Email: [email protected]

Kutlu, Onur C., MD RESIDENT | 2013 Texas Tech Univ. Health Sciences Center General Surgery Address: 3601 4th St, MS8312 Lubbock, TX 79430 Email: [email protected]

Kwon, David, MD ACTIVE | 2014 Henry Ford Health System Surgery Address: 2799 W. Grand Blvd., K-8 Surgery Detroit, MI 48202 Email: [email protected]

Lamont, Jeffrey, MD INACTIVE | 2009 Baylor Univ. Medical Center Email: [email protected]

Lampe, Pawel, MD, PhD INACTIVE | 2012 Medical Univ. of Silesia Email: [email protected]

Lapshyn, Hryhoriy, PhD RESIDENT | 2014 Univ. Hospital Freiburg Address: Hugstetterstr. 55 Freiburg, 79106 Germany Email: [email protected]




Larvin, Michael, MD ACTIVE | 2013 Univ. of Limerick Address: GEMS Room 3-021 Limerick, Ireland Email: [email protected]

Laukkarinen, Johanna, MD, PhD ACTIVE | 2014 Tampee Univ. Hospital Dept of Gastroenterology and Alimentary Tract surgery Address: Teiskontie 35 Tampere, 33520 Finland Email: [email protected]

Lavu, Harish, MD ACTIVE | 2014 Thomas Jefferson Univ. Surgery Address: 1025 Walnut St., College Bldg, Suite 605 Philadelphia, PA 19107 Email: [email protected]

Lazar, Melissa, MD INACTIVE | 2010 Thomas Jefferson Univ. Email: [email protected]

Le, Maithao, MD INACTIVE | 2011 City of Hope Email: [email protected]

Lee, Christina, MD RESIDENT | 2014 Univ. of Wisconsin Address: 600 Highland Ave. Madison, WI 53792 Email: [email protected]

Lee, Grace Clara, BS RESIDENT | 2014 Massachusetts General Hospital Dept. of Surgery Address: 10 Emerson Place, Apt. 15H Boston, MA 02114 Email: [email protected]

Lee, Jeffrey E., MD ACTIVE | 2014 UT, MD Anderson Cancer Center Dept. of Surgical Oncology Address: 1400 Pressler St., Unit 1484 Houston, TX 77030 Email: [email protected]

Lee, Kenneth K.W., MD ACTIVE | 2014 Univ. of Pittsburgh School of Medicine Dept. of Surgery Address: 497 Scaife Hall Pittsburgh, PA 15221 Email: [email protected]

Lennon, Anne Marie, MD INACTIVE | 2012 Johns Hopkins Univ. Email: [email protected]

Lesslie, III., Donald P., DO ACTIVE | 2014 Univ. of Texas - Houston Surgery Address: 6431 Fannin St., MSB 4.164 Houston, TX 77030 Email: [email protected]

Leung, Dennis MS INACTIVE | 2011 Evanston NorthShore Univ. HealthSystem Email: [email protected]

Levenson, Victor, MD INACTIVE | 2011 Email: [email protected]

Lewis, Russell RESIDENT | 2014 Perelman School of Medicine, Univ. of Pennsylvania Philadelphia, PA 19103 Email: [email protected]

Liang, Tao INACTIVE | 2012 Email: [email protected]

Lillemoe, Keith D., MD ACTIVE | 2014 Massachusetts General Hospital Dept. of Surgery Address: 55 Fruit St., WHT 506 Boston, MA 02114 Email: [email protected]

129



Linnebacher, Michael INACTIVE | 2012 Email: [email protected]

Liss, Andrew INACTIVE | 2012 Email: [email protected]

Loux, Tara, MD INACTIVE | 2011 Univ. of Pittsburgh Medical Center Email: [email protected]

Lowy, Andrew A., MD ACTIVE | 2014 UC San Diego Moores Cancer Center Surgery Address: 3855 Health Sciences Dr. ML 0987 La Jolla, CA 92093-0987 Email: [email protected]

Luffarelli, Paolo, MD RESIDENT | 2014 Campus Bio-Medico Univ. Address: via Alvaro del Portillo, 200 Rome, 00128 Italy Email: [email protected]

Ly, Quan P., MD ACTIVE | 2014 Univ. of Nebraska Medical Center Surgery Address: 986345 Nebraska Medical Center Omaha, NE 68198-4030 Email: [email protected]

Lyo, Victoria, BA INACTIVE | 2010 UCSF Email: [email protected]

Lyu, Heather, BA RESIDENT | 2013 Johns Hopkins Univ. School of Medicine Address: 1110 South Kenwood Ave. Baltimore, MD 21224 Email: [email protected]

Machado, Marcel C.C., MD ACTIVE | 2014 Univ. of Sao Paulo Faculty of Medicine Address: Peixoto Gomide 515 #134 Sao Paulo, SP 1409001 Brazil Email: [email protected]

MacKenzie, Shawn INACTIVE | 2010 Virginia Piper Cancer Institute Email: [email protected]

Magge, Deepa, MD INACTIVE | 2011 Univ. of Pittsburgh Medical Center Email: [email protected]

Magnuson, Thomas, MD ACTIVE | 2013 Johns Hopkins Dept. of Surgery Address: 4940 Eastern Ave., A558 Baltimore, MD 21224 Email: [email protected]

Mahvi, David, MD INACTIVE | 2009 Northwestern Univ. Email: [email protected]

Maithel, Shishir Kumar, MD ACTIVE | 2013 Emory Univ. Surgery, Division of Surgical Oncology, Winship Cancer Institute Address: 1365C Clifton Rd., NE, Building C, 2nd Floor Atlanta, GA 30322 Email: [email protected]

Makary, Martin INACTIVE | 2009 Johns Hopkins Email: [email protected]

Makoto, Satake, MD, PhD ACTIVE | 2014 Hyogo College of Medicine, Sasayama Med. Ctr. Dept. of Surgery Address: 5 Kurooka Sasayama, Hyogo 6692-321 Japan Email: [email protected]

Makowiec, Frank, MD ACTIVE | 2014 Univ. of Freiburg Dept. of Surgery Address: Hugstetter Strasse 55 Freiburg, D-79106 Germany Email: [email protected]




Malleo, Giuseppe, MD INACTIVE | 2012 Pioliclinico GB Rossi Verona Email: [email protected]

Mammen, Joshua, MD INACTIVE | 2009 Email: [email protected]

Manos, Lindsey, PA-C RESIDENT | 2014 Johns Hopkins Medicine Dept. of Surgery Address: 600 North Wolfe St., Halsted 600 Baltimore, MD 21287 Email: [email protected]

Mansour, John ACTIVE | 2014 Address: 5323 Harry Hines Blvd. Dallas, TX 75390-8548 Email: [email protected]

Marchegiani, Giovanni, MD RESIDENT | 2014 MGH - Harvard Medical School Address: 55 Fruit St. Boston, MA 02114 Email: [email protected]

Marcus, Stuart, MD INACTIVE | 2011 St. Vincent’s Medical Center Email: [email protected]

Marks, William H., MD, PhD INACTIVE | 2009 Swedish Medical Center Email: [email protected]

Martin, Ronald, MD ACTIVE | 2013 Marshfield Clinic Address: 1000 North Oak Ave. Marshfield, WI 54449 Email: [email protected]

Martin II., Robert C. G., MD, PhD ACTIVE | 2014 Univ. of Louisville School of Medicine Surgery/Surgical Oncology Address: 315 E. Broadway (M10) Louisville, KY 40202 Email: [email protected]

Martinie, John, MD ACTIVE | 2014 Carolinas Medical Center Surgery Address: 1025 Morehead Medical Dr., #300 Charlotte, NC 28204 Email: [email protected]

Mathur, Abhishek, MD RESIDENT | 2013 Indiana Univ. Address: 345 Bayshore Blvd., Apt. 409 Tampa, FL 33606 Email: [email protected]

Matrisian, Lynn, PhD, MBA ACTIVE | 2014 Pancreatic Cancer Action Network Research and Scientific Affairs Address: 1500 Rosencrans Ave., Suite 200 Manhattan Beach, CA 90260 Email: [email protected]

Matsubayashi, Hiroyuki, MD, PhD ACTIVE | 2013 Shizuoka Cancer Center Endoscopy Address: 1007, Shimonagakubo, Nagaizumi Suntogun, Shizuoka 411-8777 Japan Email: [email protected]

Matthews, Jeffrey B., MD ACTIVE | 2014 The Univ. of Chicago Dept. of Surgery Address: 5841 S. Maryland Ave., MC 5029 Chicago, IL 60637 Email: [email protected]

Maupin, George Capt. INACTIVE | 2009 Email: [email protected]

Mazzini, Guilherme, MD ACTIVE | 2014 Universidade Federal do Rio Grande do Sul Address: Ramiro Barcelos 2600, anexo Porto Alegre, RS 90035 Brazil Email: [email protected]

McAuliffe, John INACTIVE | 2012 Email: [email protected]

131



McDonald, Douglas R., MD RESIDENT | 2014 ETSU Surgery Address: 66 Glory Court, Jonesborough, TN 37659 Email: [email protected]

McDowell, Dena, MS, RD INACTIVE | 2011 Froedtert Hospital Email: [email protected]

McKenzie, Shawn, MD INACTIVE | 2009 City of Hope National Medical Center Email: [email protected]

McMillan, Matthew RESIDENT | 2014 Univ. of Pennsylvania School of Medicine Address: 3400 Spruce St, 4 Silverstein Philadelphia, PA 19104 Email: [email protected]

Menon, Vijay, MD RESIDENT | 2013 Cedars-Sinai Medical Center Address: 8635 W. Third St., Suite 590W Los Angeles, CA 90036 Email: [email protected]

Merchant, Nipun, MD ACTIVE | 2014 Vanderbilt Univ. Medical Center Division of Surgical Oncology Address: 2220 Pierce Ave 597 Preston Research Building Nashville, TN 37232-6860 Email: [email protected]

Mesleh, Marc, MD ACTIVE | 2014 Advocate Christ Medical Center Address: 4400 W 95th St., Suite 413 Oak Lawn, IL 60453 Email: [email protected]

Metildi, Cristina, MD, MAS RESIDENT | 2013 UC San Diego Health System Dept. of General Surgery Address: 3990 Centre St., Unit 102 San Diego, CA 92103 Email: [email protected]

Meyer, Alberto INACTIVE | 2011 USP Email: [email protected]

Mezhir, James J., MD ACTIVE | 2014 Univ. of Iowa Hospitals and Clinics Surgical Oncology Address: 200 Hawkins Drive, 4642 JCP Iowa City, IA 52242 Email: [email protected]

Michelassi, Fabrizio, MD INACTIVE | 2011 Weill Medical College of Cornell Univ. Email: [email protected]

Mier, Fernando, MD INACTIVE | 2009 ABC Medical Center Email: [email protected]

Mier, Juan, MD ACTIVE | 2014 Centro Medico ABC Surgery Address: Paseo de la Reforma 2608-1215 Mexico City, DF 11950 Mexico Email: [email protected]

Miller, Benjamin, BA RESIDENT | 2013 Email: [email protected]

Mino-Kenudson, Mari, MD ACTIVE | 2014 Massachusetts General Hospital & Harvard Medical School Pathology Address: Warren 122, 55 Fruit St. Boston, MA 02114 Email: [email protected]

Mizuno, Shugo, MD ACTIVE | 2014 Mie Univ. Address: 2-174 Edobashi Tsu City, Mie 514-0001 Japan Email: [email protected]

Mohammed, Somala, MD RESIDENT | 2014 Baylor College of Medicine Dept. of General Surgery Address: 7675 Phoenix Dr. #834 Houston, TX 77030 Email: [email protected]




Moningi, Shalini RESIDENT | 2014 Johns Hopkins School of Medicine Address: 640 N. Calvert St., Apt. A Baltimore, MD 21202 Email:

Montosori, Marco, MD ACTIVE | 2014 Univ. of Milan Address: Via Manzoni 56, Rozzano Milano, 20089 Italy Email: [email protected]

Moody, Frank G., MD ACTIVE | 2014 UT Houston Medical School Dept. of Surgery Address: 6431 Fannin St., MSB 4.130 Houston, TX 77030 Email: [email protected]

Morgan, Katy, MD ACTIVE | 2014 Medical Univ. of South Carolina Dept of Surgery Address: 25 Courtenay Dr., Suite 710, MSC 290 Charleston, SC 29425 Email: [email protected]

Moritz, Katharina, Dr. INACTIVE | 2011 Universitätsklinikum Rostock Email: [email protected]

Moriya, Toshiyuki, MD, PhD ACTIVE | 2014 Okitama Public General Hospital Address: 2000 Nishi-Otsuka Kawanishi-Machi, Yamagata 992-0601 Japan Email: [email protected]

Moser, Arthur James, MD ACTIVE | 2014 BIDMC Surigical Oncology Address: 330 Brookline Ave Boston, MA 02215 Email: [email protected]

Muilenburg, Diego, MD INACTIVE | 2009 Univ. of California at Davis Email: [email protected]

Mulvihill, Sean J., MD ACTIVE | 2014 Univ. of Utah Medical Group Dept. of Surgery Address: 175 N Medical Drive East, Room 5223 Salt Lake City, UT 84132-2301 Email: [email protected]

Murata, Yasuhiro, MD INACTIVE | 2012 Mie Univ. Email: [email protected]

Murr, Michel M., MD ACTIVE | 2014 USF- Tampa General Hospital Bariatric Center Dept. of Surgery Address: 5 Tampa General Circle, Suite 410 Tampa, FL 33606 Email: [email protected]

Muscarella, II, Peter, MD ACTIVE | 2014 Ohio State Univ. Surgery Address: N711 Doan Hall, 410 West 10th Ave. Columbus, OH 43210 Email: [email protected]

Nadeau, Laura, MD INACTIVE | 2011 William Beaumont Hospital Email: [email protected]

Nagorney, David M., MD ACTIVE | 2014 Mayo Clinic College of Medicine Subspecialty General Surgery Address: 200 First St. SW Rochester, MN 55905 Email: [email protected]

Nakagawa, Naoya, MD RESIDENT | 2013 Hiroshima Univ. Address: 1-2-3 Kasumi, MInami-ku Hiroshima, Hiroshima 734-8551 Japan Email: [email protected]

133



Nakamura, Masafumi, MD, PhD ACTIVE | 2013 Address: Matsushima 577, 701-0192 Kurashiki, Japan Email: [email protected]

Nakashima, Akira, MD INACTIVE | 2010 Hiroshima Univ. Email: [email protected]

Nakeeb, Attila, MD ACTIVE | 2014 Indiana Univ. School of Medicine Dept. of Surgery Address: 539 Emerson Hall Indianapolis, IN 46202 Email: [email protected]

Nappo, Gennaro, MD RESIDENT | 2014 Univ. Campus Bio-Medico di Roma General Surgery Address: Via Alvaro Del Potillo, 200 Rome, 00128 Italy Email: [email protected]

Narra, Vinod, MD INACTIVE | 2009 Henry Ford Hospital Email: [email protected]

Naru, Kondo, MD INACTIVE | 2010 Hiroshima Univ. Email: [email protected]

Nathan, Hari, MD INACTIVE | 2009 Johns Hopkins Univ. Email: [email protected]

Nealon, William H., MD ACTIVE | 2014 Vanderbilt Univ. School of Medicine General Surgery Address: 1161 Medical Center Dr., D5203 MCN Nashville, TN 37232-2577 Email: [email protected]

Neeff, Hannes P., MD ACTIVE | 2014 Univ. Hospital Freiburg General and Digestive Surgery Address: Hugstetterstr. 55 Freiburg, 79106 Germany Email: [email protected]

Newhook, Timothy, MD RESIDENT | 2014 Univ. of Virginia Dept. of Surgery Address: PO Box 800679 Charlottesville, VA 22908 Email: [email protected]

Nguyen, Andrew RESIDENT | 2014 UCLA Address: 1730 Sawtelle Blvd. #307, Los Angeles, CA 90025 Email: [email protected]

Nguyen, Katherine, MD INACTIVE | 2009 Thomas Jefferson Univ. Email: [email protected]

Nguyen, Trang, MD RESIDENT | 2014 Univ. of Pittsburgh Address: 425 N. Neville St., Apt 102 Pittsburgh, PA 15213 Email: [email protected]

Niccola, Funel INACTIVE | 2012 Email: [email protected]

Nicholl, Michael B., MD ACTIVE | 2014 Univ. of Missouri Dept. of Surgery Address: One Hospital Drive, MC 520E Columbia, MO 65212 Email: [email protected]

Nichols, R. Charles, MD ACTIVE | 2014 UF Proton Therapy Institute Radiation Oncology Address: 2015 North Jefferson St. Jacksonville, FL 32206 Email: [email protected]

Nijmeijer, Rian INACTIVE | 2009 Email: [email protected]




Nikfarjam, Mehrdad, MD, PhD, FRACS ACTIVE | 2014 Univ. of Melbourne, Austin Health Surgery Address: LTB 8, 145 Studley Rd. Heidelberg Melbourne, VIC 3084 Australia Email: [email protected]

Nissen, Nicholas, MD ACTIVE | 2013 Cedars-Sinai Medical Center Dept. of Surgery Address: 8635 W. Third St., Suite 590 Los Angeles, CA 90048 Email: [email protected]

Nubuoka, Yu, MD INACTIVE | 2009 Mie Univ. Graduate School of Medicine Email: [email protected]

Nussbaum, Michael S., MD ACTIVE | 2014 Univ. of Florida COM Dept. of Surgery Address: 653 W. 8th St., 3rd Floor Faculty Clinic Jacksonville, FL 32209 Email: [email protected]

Okada, Toshihiro, MD, PhD INACTIVE | 2011 Hyogo College of Medicine Email: [email protected]

Okuda, Yoshihiro, MD RESIDENT | 2014 Email: [email protected]

Olino, Kelly, MD INACTIVE | 2010 The Johns Hopkins Hospital Email: [email protected]

Onetti Muda, Andrea, MD ACTIVE | 2013 Campus Bio-Medico Univ. of Rome Dept. of Pathology Address: Via Alvaro del Portillo, 200, Rome, 00128 Italy Email: [email protected]

Ongchin, Melanie, MD RESIDENT | 2014 Email: [email protected]

Orr, Shannon, MD INACTIVE | 2011 Univ. of Tennessee Health Science Center Email: [email protected]

Osvaldt, Alessandro, MD, PhD ACTIVE | 2014 Hospital de Clinicas de Porto Alegre Address: Cristovao Colombo, 3060, Porto Alegre, RS 90035-170 Brazil Email: [email protected]

Otsuka, Takao, MD, PhD ACTIVE | 2014 Kyushu Univ. Dept. of Surgery and Oncology Address: 3-1-1 Maidashi, Higashi-ku Fukuoka, 812-8582 Japan Email: [email protected]

Ouellet, Jean-Francois INACTIVE | 2012 Email: [email protected]

Ouellette, James DO INACTIVE | 2009 Wright State Univ. Email: [email protected]

Ovrebo, Kjell, MD INACTIVE | 2010 Haukeland Univ. Hospital Email: [email protected]

Paniccia, Alessandro INACTIVE | 2012 Email: [email protected]

Panni, Roheena, MD RESIDENT | 2014 St. Louis, MO 63108 Email: [email protected]

Papalezova, Katia, MD INACTIVE | 2010 Duke Univ. Medical Center Email: [email protected]

Papavasiliou, Pavlos, MD INACTIVE | 2011 Fox Chase Cancer Center Email: [email protected]

135



Pappas, Theodore N., MD INACTIVE | 2010 Duke Univ. Medical Center Email: [email protected]

Pappas, Sam, MD ACTIVE | 2014 Loyola Univ. Medical Center General Surgery Address: 2160 S. First Ave. Maywood, IL 60153 Email: [email protected]

Parasher, Gulshan, MD INACTIVE | 2011 Univ. of New Mexico Email: [email protected]

Parekh, Dilip, MD INACTIVE | 2009 Univ. of Southern California Email: [email protected]

Parikh, Alexander, MD ACTIVE | 2014 Vanderbilt Univ. Medical Center Surgical Oncology Address: 2220 Pierce Ave., 597 PRB Nashville, TN 37232 Email: [email protected]

Parikh, Purvi Y., MD ACTIVE | 2014 Address: 7 Keats Common, Slingerlands, NY 12159 Email: [email protected]

Parikh, Janak, MD, MSHS ACTIVE | 2014 St. John Providence Address: 26850 Providence Parkway, Suite 504 Novi, MI 48374 Email: [email protected]

Park, Joo Kyung, MD INACTIVE | 2009 Seoul National Univ. Hospital Email: [email protected]

Parmar, Abhishek, MD RESIDENT | 2013 UCSF-East Bay, UTMB Address: 2902 Chenevert St., Unit K Houston, TX 77004 Email: [email protected]

Partelli, Stefano, MD INACTIVE | 2011 Univ. of Verona Email: [email protected]

Paulus, Elena, MD INACTIVE | 2011 Univ. of Tennessee Health Science Center Email: [email protected]

Pawlik, Timothy, MD, PhD ACTIVE | 2014 Johns Hopkins Univ. Surgery Address: 600 N. Wolfe St., Blalock 665 Baltimore, MD 21287 Email: [email protected]

Pek, Chulja INACTIVE | 2009 Email: [email protected]

Pellegrini, Carlos A., MD RETIRED/HONORARY | 2009 Univ. of Washington Dept. of Surgery Address: 1959 NE Pacific St., Box 356410 Seattle, WA 98195-6410 Email: [email protected]

Peng, June RESIDENT | 2014 Cleveland Clinic Address: 9500 Euclid Ave. Cleveland, OH 44195 Email: [email protected]

Penteado, Sonia, MD ACTIVE | 2014 Hospital das Clinicas FM VSP Gastroenterology Address: rua Cristiano Viana 1089/11 Sao Paulo, 05411-002 Brazil Email: [email protected]

Perrone, Giuseppe, MD ACTIVE | 2013 Campus Bio-Medico Univ. Pathology Address: Via Alvaro del Portillo, 200 Rome, 00128 Italy Email: [email protected]




Perrone, Vittorio Grazio, MD INACTIVE | 2009 Chirurgia Univ. Email: [email protected]

Petzel, Maria, BS, RD INACTIVE | 2012 MD Anderson Cancer Center Email: [email protected]

Pham, Hung, PhD INACTIVE | 2009 UCLA David Geffen School of Medicine Email: [email protected]

Pilgrim, Charles, MD, PhD RESIDENT | 2013 Medical College of Wisconsin Address: 9200 W Wisconsin Ave. Milwaukee, WI 53226 Email: [email protected]

Pimiento, Jose, MD INACTIVE | 2012 Moffitt Cancer Center Email: [email protected]

Pineda, Danielle INACTIVE | 2012 Email: [email protected]

Pinson, C. Wright, MD INACTIVE | 2009 Vanderbilt Univ. Email: [email protected]

Pitt, Henry, MD ACTIVE | 2014 Temple Univ. School of Medicine Dept. of Surgery Address: 3509 N. BRd St., Boyer Pavilion 9th Floor Rm E938 Philadpelphia, PA 19140 Email: [email protected]

Plichta, Jennifer, MD, MS RESIDENT | 2014 Loyola Univ. Medical Center General Surgery Address:: 2160 S. First Ave., EMS Bldg Maywood, IL 60153 Email: [email protected]

Polanco, Patricio, MD RESIDENT | 2014 Univ. of Pittsburgh Medical Center Address: 507 Maryland Ave. Pittsburgh, PA 15232 Email: [email protected]

Pollina, Luca Emanuele, MD INACTIVE | 2010 Hospital-Univ. of Pisa Email: [email protected]

Porpiglia, Andrea, MD RESIDENT | 2014 Fox Chase Cancer Center Address: 333 Cottman Ave., H3-133 Philadelphia, PA 19111 Email: [email protected]

Postier, Russell, MD ACTIVE | 2014 Univ. of Oklahoma College of Medicine Dept. of Surgery Address: PO Box 26901 - Williams Pavillion Room 2140 Oklahoma City, OK 73126 Email: [email protected]

Prejeant, Kristi, MD INACTIVE | 2010 Univ. of Oklahoma Health Science Ctr. Email: [email protected]

Prinz, Richard A., MD ACTIVE | 2014 NorthShore Univ. HealthSystem Dept. of Surgery Address: 2650 Ridge Ave. Walgreen 2507 Evanston, IL 60201 Email: [email protected]

Pucci, Michael J., MD ACTIVE | 2014 Jefferson Univ. Physicians Dept. of Surgery Address: 1100 Walnut St., Suite 500 Philadelphia, PA 19107 Email: [email protected]

Pupine, Aiste, MD INACTIVE | 2011 Hospital of Lithuanian Univ. of Health Sciences Email: [email protected]

137



Purich, Edward, PhD ACTIVE | 2013 ChiRhoClin, Inc. Address: 4000 Blackburn Lane, Suite 270 Burtonsville, MD 20866 Email: [email protected]

Que, Florencia G., MD ACTIVE | 2014 Mayo Clinic Dept. of Surgery Address: 200 First St. SW Rochester, MN 55905 Email: [email protected]

Rabiee, Atoosa, MD INACTIVE | 2009 Johns Hopkins Bayview Email: [email protected]

Ragulin Coyne, Elizaveta, MD, MHS INACTIVE | 2012 UMASS Medical School Email: [email protected]

Raigani, Siavash, BA RESIDENT | 2013 CWRU School of Medicine Address: 2300 Overlook Rd., Apt. 717 Cleveland, OH 44106 Email: [email protected]

Rao, Bettina, Prof. INACTIVE | 2009 Univ. of Rostock Email: [email protected]

Raoof, Mustafa INACTIVE | 2012 Email: [email protected]

Raper, Steven E., MD INACTIVE | 2009 Email: [email protected]

Rasmussen, Ib C., MD, PhD ACTIVE | 2014 Falun County Hospital Dept. of Surgery Address: Hurtigs gata 23 2tr Falun, SE-79182 Sweden Email: [email protected]

Reber, Howard, MD ACTIVE | 2014 UCLA School of Medicine Address: 10833 LeConte Ave. Los Angeles, CA 90095 Email: [email protected]

Reddy, Sanjay S., MD ACTIVE | 2014 Fox Chase Cancer Center Address: 333 Cottman Ave. Philadelphia, PA 19111 Email: [email protected]

Reddy, Sushanth, MD INACTIVE | 2010 Johns Hopkins Univ. Email: [email protected]

Reid Lombardo, Kaye M., MD ACTIVE | 2014 Mayo Clinic Dept. of Surgery Address: 200 First St. SW Rochester, MN 55905 Email: [email protected]

Relles, Daniel, MD RESIDENT | 2013 Jefferson Address: 1015 Walnut St. Suite 620 Philadelphia, PA 19107 Email: [email protected]

Rezaee, Neda, MD RESIDENT | 2014 Johns Hopkins Univ. Address: 600 North Wolfe St., Blalock 1206 Baltimore, MD 21287 Email: [email protected]

Riall, Taylor S., MD, PhD ACTIVE | 2014 Univ. of Texas Medical Branch Dept. of Surgery Address: 301 Univ. Blvd., JSA 6.110c Galveston, TX 77555-0541 Email: [email protected]

Richards, Nathan, MD INACTIVE | 2010 Thomas Jefferson Univ. Email: [email protected]




Richter, Harry, MD ACTIVE | 2014 Stroger Hospital of Cook County Dept. of Surgery Address: 1901 W Harrison St. Chicago, IL 60612 Email: [email protected]

Rilo, Horacio, MD INACTIVE | 2011 Univ. of Arizona Email: [email protected]

Rittenhouse, David, MD INACTIVE | 2011 Thomas Jefferson Univ. Email: [email protected]

Robinson, Jamie, MD RESIDENT | 2014 Vanderbilt Univ. Medical Center Dept of Surgery Address: 1161 21st Ave. S, D-4314 MCN Nashville, TN 37232-2730 Email: [email protected]

Rocha, Flavio, MD ACTIVE | 2013 Address: 1100 9th Ave. Seattle, WA 98101 Email: [email protected]

Rochefort, Matthew INACTIVE | 2012 Email: [email protected]

Roggin, Kevin, MD INACTIVE | 2011 Univ. of Chicago Email: [email protected]

Roland, Christina, MD RESIDENT | 2013 MD Anderson Cancer Center Email: [email protected]

Ronnekleiv-Kelly, Sean, MD RESIDENT | 2013 Univ. of Wisconsin Hospital and Clinics Address: Dept. of Surgery, 600 Highland Ave. Madison, WI 53792 Email: [email protected]

Rosati, Carlo M., MD INACTIVE | 2011 Scuola Superiore Sant’Anna Email: [email protected]

Rosati, Lauren RESIDENT | 2014 Address: 7709 Takoma Ave. Takoma Park, MD 20912 Email: [email protected]

Rose, J. Bart, MD, MAS RESIDENT | 2013 Virginia Mason Medical Center GME Address: 1100 9th Ave. Seattle, WA 98101 Email: [email protected]

Rosemurgy, Alexander S., MD ACTIVE | 2014 Florida Hospital Tampa Surgery Address: 3000 Medical Park Drive #310, Tampa, FL 33613 Email: [email protected]

Rosen, Matthew Marc, MD INACTIVE | 2009 Thomas Jefferson Univ. Email: [email protected]

Rosenberg, Lawrence, MD ACTIVE | 2014 Jewish General Hospital- McGill Univ. Surgery Address: 3755 Lote Sarinthe Catherine Suite B-119 Montreal, QC H2T1E3 Canada Email: [email protected]

Rosenberg, Wade, MD INACTIVE | 2010 Texas Surgical Associates Email: [email protected]

Ross, Sharona B., MD, FACS ACTIVE | 2014 Florida Hospital Tampa Surgery Address: 3000 Medical Park Drive, Suite 310 Tampa, FL 33613 Email: [email protected]

139



Roy, Ishan INACTIVE | 2011 Medical College of Wisconsin Email: [email protected]

Royal, Richard E., MD ACTIVE | 2013 MD Anderson Cancer Center Address: 1400 Pressler Drive, Unit 1484 Houston, TX 77030 Email: [email protected]

Rupp, Christopher, MD INACTIVE | 2011 Univ. of NC Chapel Hill Email: [email protected]

Sachdeva, Ashwin INACTIVE | 2009 Newcastle Univ. Email: [email protected]

Sagi, Sashidhar INACTIVE | 2012 Email: [email protected]

Sah, Raghuwansh INACTIVE | 2011 Univ. of Minnesota Email: [email protected]

Saif, Wasif, MD, MBBS ACTIVE | 2014 Tufts Univ. School of Medicine Tufts Cancer Center Address: 800 Washington St. Suite 7099 7South Boston, MA 02111 Email: [email protected]

Sakabe, Ryutaro, MD INACTIVE | 2011 Hiroshima Univ. Email: [email protected]

Sakata, Naoaki, MD, HD INACTIVE | 2009 Loma Linda Univ. Email: [email protected]

Saldinger, Pierre F., MD ACTIVE | 2013 New York Hospital Queens Surgery Address: 56-45 Main St. Flushing, NY 11355 Email: [email protected]

Salem, Ahmed Farouk, PhD INACTIVE | 2009 Univ. of Pisa & Thomas Jefferson Email: [email protected]

Salman, Bulent, MD ACTIVE | 2013 John Hopkins Surgery Address: 600 N. Wolfe St., 1206 Blalock Baltimore, MD 21287 Email: [email protected]

Saluja, Ashok K., PhD ACTIVE | 2014 Univ. of Minnesota Surgery, Basic & Translational Research Address: 420 Delaware St. SE, MMC 195 Minneapolis, MN 55455 Email: [email protected]

Samuel, Isaac, MD INACTIVE | 2011 Univ. of Iowa Email: [email protected]

Sanabria, Juan, MD, MSc, FRCSC ACTIVE | 2014 Case Western Reserve Univ., Cancer Treatment Centers of America Surgery, Nutrtion & Preventive Medcine Address: 3239 Bremerton Rd. Pepper Pike, OH 44124 Email: [email protected]

Sanchez, Norberto, MD INACTIVE | 2011 Beth Isreal Deaconess MC Email: [email protected]

Sand, Juhani, MD, PhD INACTIVE | 2011 Tampere Univ. Hospital Email: [email protected]

Sanford, Dominic, MD RESIDENT | 2013 Washington Univ. School of Medicine Address: 4531 Westminster Place St. Louis, MO 63108 Email: [email protected]

Santos Sousa, Hugo, MD, MSc INACTIVE | 2012 Centro Hospitalar de São João Univ. of Porto Faculty of Medicine Email: [email protected]




Sarmiento, Juan M., MD ACTIVE | 2014 Emory Univ. Hospital Dept. of Surgery Address: 1365 Clifton Rd. NE, Suite A5039 Atlanta, GA 30322 Email: [email protected]

Sarosiek, Konrad, MD RESIDENT | 2013 Thomas Jefferson Address: 201 N 8th St. Unit 314 Philadelphia, PA 19106-1011 Email: [email protected]

Sarr, Michael G., MD ACTIVE | 2014 Mayo Clinic Gastroenterology Research Unit Address: 200 1st St. SW Rochester, MN 55905 Email: [email protected]

Sasaki, Hayato, MD RESIDENT | 2014 Hiroshima Univ. Address: 1-2-3 Kasumi, Minami-ku Hiroshima, 734-8551 Japan Email: [email protected]

Sassatani, Alexandre, MD INACTIVE | 2009 Santa Casa Medical School Email: [email protected]

Sasson, Aaron R., MD ACTIVE | 2014 Univ. of Nebraska Medical Center Dept. of Surgery Address: 986345 Nebraska Medical Center Omaha, NE 68198-6345 Email: [email protected]

Satoi, Sohei, MD, FACS ACTIVE | 2014 Kansai Medical Univ. Dept. of Surgery Address: 2-5-1, Shin-machi, Hirakata OSAKA, 573-1010 Japan Email: [email protected]

Scaife, Courtney, MD ACTIVE | 2014 Univ. of Utah/ Huntsman Cancer Institute General Surgery Address: 1950 Circle of Hope, Suite N6405 Salt Lake City, UT 84132 Email: [email protected]

Schellhaas, Elisabeth, MD INACTIVE | 2009 Charite Medical School Email: [email protected]

Schiller, William R., MD ACTIVE | 2014 Southern Illinois Univ. - SOM Surgery Address: 784 Aspen Compound, Santa Fe, NM 87501 Email: [email protected]

Schmidt, C. Max ACTIVE | 2013 Address: 550 N Univ. Blvd. Indianapolis, IN 46202 Email: [email protected]

Schneider, Patrick INACTIVE | 2009 Penn State College of Medicine Email: [email protected]

Schulick, Richard, MD INACTIVE | 2011 Email: [email protected]

Schwandner, Frank INACTIVE | 2011 Univ. of Rostock Email: [email protected]

Schwarz, Roderich, MD, PhD ACTIVE | 2014 Indiana Univ. Health Goshen Center for Cancer Care Address: 200 High Park Ave Goshen, IN 46526-4810 Email: [email protected]

Schwesinger, Wayne H., MD INACTIVE | 2009 The Univ. of Texas HSC at San Antonio Email: [email protected]

Sclabas, Guido, MD INACTIVE | 2011 Mayo Clinic Email: [email protected]

Scognamiglio, Pasquale RESIDENT | 2014 Campus Bio-Medico Univ. of Rome Address: Via Alvaro del Portillo, 200 Rome, 00128 Italy Email: [email protected]

141



Scow, Jeffrey S., MD INACTIVE | 2010 Mayo Clinic Email: [email protected]

Seifert, Hans, MD ACTIVE | 2013 Carl von Ossietzky Universität Gastroenterology and Hepatology Address: Rahel Straus Str. 10 Oldenburg, 26131 Germany Email: [email protected]

Serrano, Pablo, MD ACTIVE | 2014 McMaster Univ. Surgery Address: 711 Concession St., B3-161 Hamilton, ON L8V1C3 Canada Email: [email protected]

Seshadri, Ramanathan, MD RESIDENT | 2014 Carolinas Medical Center Address: 1025 Morehead Medical Drive, Suite 600 Huntersville, NC 28078 Email: [email protected]

Sethi, Saurabh, MD, MPH INACTIVE | 2009 Wayne State Univ. Detroit MC Email: [email protected]

Sewryn, Mariusz MSN RESIDENT | 2013 Slielsian Medical Univ. Address: Pck 10 Sosnowiec, 41-200 Poland Email: [email protected]

Shah, Paresh, MD ACTIVE | 2013 Lenox Hill Hospital Address: 186 east 76th St. new york, NY 10075 Email: [email protected]

Shah, Rupen, MD INACTIVE | 2011 Henry Ford Hospital Email: [email protected]

Sharp, Kenneth W., MD ACTIVE | 2014 Vanderbilt Univ. Medical Center Dept. of Surgery Address: D5203 MCN Nashville, TN 37232-2577 Email: [email protected]

Sharpe, Susan, MD RESIDENT | 2014 Univ. of Chicago Address: 5841 South Maryland Ave, MC-6040 Chicago, IL 60637 Email: [email protected]

Shaw, Christiana, MD INACTIVE | 2010 Fox Chase Cancer Center Email: [email protected]

Shea, Jill, MD, PhD ACTIVE | 2013 Univ. of Utah Dept. of Surgery Address: 1950 Circle of Hope, Ste. HCH N6405 Salt Lake City, UT 84132 Email: [email protected]

Shelton, Julia INACTIVE | 2012 Email: [email protected]

Sheppard, Brett C., MD ACTIVE | 2014 Oregon Health & Sciences Univ. Division of General Surgery Address: 3181 SW Sam Jackson Park Rd Mail Code: L223A Portland, OR 97239 Email: [email protected]

Sherman, Karen INACTIVE | 2012 Email: [email protected]

Shi, Jun INACTIVE | 2012 Email: [email protected]

Shimizu, Shuji, MD INACTIVE | 2011 Kyushu Univ. Hospital Email: [email protected]




Shin, Marcus PhD ACTIVE | 2014 Forest Labs Medical Affairs Address: 6510 Ocean Crest Dr. Apt. C109 Rancho Palos Verdes, CA 90275 Email: [email protected]

Shoup, Margo, MD ACTIVE | 2014 Cadence Cancer Center at Warrenville Surigical Oncology Address: 4405 Weaver Parkway Warrenville, IL 60555 Email: [email protected]

Showalter, Shayna, MD INACTIVE | 2009 Thomas Jefferson Univ. Email: [email protected]

Shuford, Betsy RN ACTIVE | 2013 Medical Univ. of South Carolina Address: 25 Courtenay Dr., Suite 7100 A Charleston, SC 29425 Email: [email protected]

Shukla, Parul, MD INACTIVE | 2009 TATA Memorial Hospital Email: [email protected]

Siecean, Andrada, MD, PhD INACTIVE | 2009 Univ. of Medicine & Pharmacy Email: [email protected]

Siripurapu, Veeraiah, MD INACTIVE | 2011 Fox Chase Medical Center Email: [email protected]

Smith, Kerrington D., MD ACTIVE | 2014 Dartmouth Hitchcock Medical Center Surgery Address: One Medical Center Drive Lebanon, NH 03756 Email: [email protected]

Smith, Jillian K., MD, MPH INACTIVE | 2011 Univ. of Massachusetts Medical School Email: [email protected]

Solorzano, Carmen C., MD INACTIVE | 2009 Sylvester Cancer Center Email: [email protected]

Solotkin, Kathleen MSN INACTIVE | 2011 Eli Lilly and Company Email: [email protected]

Soriano, Perry A., MD INACTIVE | 2009 Everett Clinic Email: [email protected]

Spencer, Philip INACTIVE | 2011 Massachusetts General Hospital Email: [email protected]

Spitzer, Austin INACTIVE | 2012 Email: [email protected]

Squires, Malcolm Hart, MD RESIDENT | 2013 Emory Univ. Dept. of Surgery, Div. of Surgical Oncology Address: 865 Fraser St. SE Atlanta, GA 30315 Email: [email protected]

Stauffer, John, MD ACTIVE | 2014 Mayo Clinic Address: 4500 San Pablo Rd. Jacksonville, FL 32224 Email: [email protected]

Stein, Julie Ann, MD INACTIVE | 2011 William Beaumont Hospital Email: [email protected]

Stephens, Robert V., MD RETIRED/HONORARY | 2011 Dept. of Surgery Address: 2320 E. Marshall Phoenix, AZ 85016 Email: [email protected]

StLaudereas, Styestovia Yestee, PhD INACTIVE | 2012 Methodist Hospital -Vascular Surgeries Email: [email protected]

143



Strasberg, Steven M., MD ACTIVE | 2014 Washington Univ. School of Medicine Surgery Address: 660 S Euclid Ave, Campus Box 8109 St. Louis, MO 63110 Email: [email protected]

Strohl, Madeleine RESIDENT | 2014 Email: [email protected]

Sugimoto, Motokazu, MD RESIDENT | 2014 St. Luke’s Health System Address: 100 East Idaho St., Suite 301 Boise, ID 83712 Email: [email protected]

Sugiura, Teiichi, MD, PhD INACTIVE | 2011 Shizuoka Cancer Center Email: [email protected]

Sutton, Jeffrey, MD RESIDENT | 2014 Univ. of Cincinnati College of Medicine Address: 231 Albert Sabin Way, ML 0558, SRU 1588 Cincinnati, OH 45267 Email: [email protected]

Swanson, Richard S., MD ACTIVE | 2014 Brigham & Women’s Hospital Surgery Address: 75 Francis St Boston, MA 02115 Email: [email protected]

Takaori, Kyoichi “Tony”, MD ACTIVE | 2014 Kyoto Univ. Dept. of Surgery Address: 54 Kawara-cho, Shogoin, Sakyo-ku Kyoto, Kyoto 606-8507 Japan Email: [email protected]

Talamini, Mark, MD ACTIVE | 2013 Univ. of CA SD Dept. of Surgery Address: 200 W. Arbor Drive, MC 8400 San Diego, CA 92103-8400 Email: [email protected]

Talamonti, Mark S., MD ACTIVE | 2014 NorthShore Univ. HealthSystem Division of Surgical Oncology Address: 2650 Ridge Ave., Walgreen 2507 Evanston, IL 60201 Email: [email protected]

Talbott, Vanessa, MD INACTIVE | 2011 Thomas Jefferson Univ. Email: [email protected]

Talley, Anitra BS INACTIVE | 2012 Pancreatic Cancer Action Network Email: [email protected]

Tamirisa, Nina, MD RESIDENT | 2014 Univ. of Texas Medical Branch in Galveston Email: [email protected]

Tanaka, Masao, MD, PhD ACTIVE | 2014 Kyushu Univ. Surgery and Oncology Address: 3-1-1 Maidashi Fukuoka, 812-8582 Japan Email: [email protected]

Tanaka, Shoichiro, MD RESIDENT | 2013 Address: 1514 Jefferson Hwy. New Orleans, LA 70121 Email: [email protected]

Tapper, Elliot, MD INACTIVE | 2009 Beth Israel Deaconess Email: [email protected]

Thayer, Sarah, MD, PhD INACTIVE | 2012 Mass General Hospital Email: [email protected]

Theruvath, Tom, MD, PhD INACTIVE | 2011 Medical Univ. of South Carolina Email: [email protected]

Tholey, Renee, MD RESIDENT | 2013 Thomas Jefferson Univ. Hospital Address: 1015 Walnut St Philadelphia, PA 19107 Email: [email protected]




Thomas, Ryan INACTIVE | 2012 Email: [email protected]

Thomay, Alan INACTIVE | 2012 Email: [email protected]

Thompson, Lee W., MD ACTIVE | 2014 IMC-Cancer Surgery of Mobile, P.C. Surgical Oncology Address: 3 Mobile Infirmary Circle, Suite 305 Mobile, AL 36607 Email: [email protected]

Thompson, Geoffrey, MD INACTIVE | 2011 Mayo Clinic Email: [email protected]

Toledo, Sergio, MD ACTIVE | 2013 Oregon Health & Science Univ. Address: 3181 SW Sam Jackson Park Rd. Mail Code: L223A Portland, OR 97239 Email: [email protected]

Toomey, Paul, MD RESIDENT | 2014 Univ. South Florida Surgery Address: 4246 53rd Ave. S St Petersburg, FL 33711 Email: [email protected]

Toste, Paul, MD RESIDENT | 2014 UCLA Address: 10833 Le Conte, 72-229 CHS Los Angeles, CA 90095 Email: [email protected]

Tran Cao, Hop, MD RESIDENT | 2014 U.T., MD Anderson Cancer Center Address: 1400 Pressler St., FCT 17.5000 Houston, TX 77030 Email: [email protected]

Traverso, William, MD ACTIVE | 2014 St. Luke’s Hospital System Center for Pancreatic Disease Address: 100 East Idaho St., Suite 301 Boise, ID 83616 Email: [email protected]

Trevino, Jose G., MD ACTIVE | 2014 Univ. of Florida-Gainesville Address: 1600 SW Archer Rd., Rm. 6164 Gainesville, FL 32610 Email: [email protected]

Truty, Mark, MD, MSc INACTIVE | 2012 Email: [email protected]

Tsai, Susan, MD, MHS ACTIVE | 2014 Medical College of Wisconsin Address: 9200 W Wiscinsin Ave. Milwaukee, WI 53226 Email: [email protected]

Tseng, DSJ, MD RESIDENT | 2013 Univ. Medical Center Utrecht Address: Heidelberglaen 100 Utrecht, Netherlands Email: [email protected]

Tseng, Jennifer F., BS, AB, MD, MPH ACTIVE | 2014 Beth Israel Deaconess Medical Center Surgery Address: 330 Brookline Ave., Stoneman Bldg 9th Floor, Room 913 Boston, MA 02115 Email: [email protected]

Tseng, Warren, MD INACTIVE | 2009 Univ. of California, Davis Email: [email protected]

Tsiotos, Gregory, MD INACTIVE | 2011 Metropolitan Hospital Email: [email protected]

Tzeng, Ching-Wei, MD ACTIVE | 2014 Univ. of Kentucky Address: 800 Rose St., UKMC C212 Lexington, KY 40536 Email: [email protected]

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Uemura, Kenichiro, MD ACTIVE | 2014 Hiroshima Univ. Dept. of Surgery Address: 1-2-3 Kasumi, Minamiku, Nishikasumi Hiroshima, 7348551 Japan Email: [email protected]

Ujiki, Michael, MD INACTIVE | 2009 Northshore Health System Email: [email protected]

Valeri, Sergio, MD INACTIVE | 2011 Univ. Campus Bio-Medico di Roma Email: [email protected]

Valero, III, Vicente, MD RESIDENT | 2014 Johns Hopkins Univ. Address: 314 Murdock Rd. Baltimore, MD 21212 Email: [email protected]

Valsangkar, Nakul, MD INACTIVE | 2012 Massachusetts General Hospital Email: [email protected]

Van Brunschot, Sandra, MD INACTIVE | 2012 Radboud Univ. Nijmegen Medical Center Email: [email protected]

Van Buren, II, George, MD ACTIVE | 2014 The Elkins Pancreas Center, Michael E. DeBakey Address: 6620 Main St, Suite 1350 Houston, TX 77030 Email: [email protected]

Van Cott, Christine E., MD ACTIVE | 2013 St. Vincents Medical Center Dept. of Surgery/Oncology Address: 2800 Main St., 3rd Floor Cancer Center Bridgeport, CT 06606 Email: [email protected]

Van Eijch, Casper, MD, PhD INACTIVE | 2012 Erasmus Email: [email protected]

van Sanvoort, Hjalmar, MD INACTIVE | 2009 Univ. Medical Center Utrecht Email: [email protected]

Vanderveen, Kimberly, MD INACTIVE | 2009 Mayo Clinic Email: [email protected]

VanLier Ribbink, Jeff, MD INACTIVE | 2009 Scottsdale Healthcare Email: [email protected]

Varadarajulu, Shyam S., MD ACTIVE | 2014 Florida Hospital Center for Interventional Endoscopy Address: 601 East Rollins St. Orlando, FL 34786 Email: [email protected]

Vege, Santhi S., MD ACTIVE | 2014 Mayo Clinic Foundation Gastroenterology and Hepatology Address: 200 First St. SW, Rochester, MN 55905 Email: [email protected]

Velanovich, Vic, MD ACTIVE | 2014 Univ. of South Florida Dept. of Surgery Address: One Tampa General Circle, F145 Tampa, FL 33606 Email: [email protected]

Venkat, Raghunandan, MD, MPH INACTIVE | 2011 Johns Hopkins Medical Institution Email: [email protected]

Verzaro, Roberto M., MD INACTIVE | 2011 Vannini Hospital Rome Email: [email protected]

Vickers, Selwyn, MD INACTIVE | 2010 Univ. ofMN Email: [email protected]

Vietsch, Eveline E., MD INACTIVE | 2012 Georgetown Univ. Email: [email protected]




Villatoro, Edwardo, MD INACTIVE | 2009 Queen’s Medical Center Email: [email protected]

Visser, Brendan C., MD ACTIVE | 2014 Stanford Univ. General Surgery Address: 300 Pasteur Drive, H3680 Stanford, CA 94305-5655 Email: [email protected]

Vlada, Adrian MB BCh RESIDENT | 2013 Univ. of Florida Address: 1600 SW Archer Rd., Gainesville, FL 32610 Email: [email protected]

Vollmer, Charles M., MD ACTIVE | 2014 Univ. of Pennsylvania School of Medicine Dept. of Surgery Address: 3400 Spruce St., Silverstein Pavilion Philadelphia, PA 19103 Email: [email protected]

Volpe, Carmine, MD INACTIVE | 2011 Univ. of Florida-Jacksonville Email: [email protected]

von Holzen, Urs, MD INACTIVE | 2009 Fox Chase Cancer Center Email: [email protected]

Vyas, Ojas, MD RESIDENT | 2014 Tufts Address: 18 Bay State Ave. #1 Somerville, MA 02144 Email: [email protected]

Wada, Keita, MD ACTIVE | 2013 Teikyo Univ. Dept. of Surgery Address: 2-11-1 Kaga, Itabashi-ku Tokyo, 165-0025 Japan Email: [email protected]

Walsh, R. Matthew, MD ACTIVE | 2014 The Cleveland Clinic Foundation Dept. of General Surgery Address: 9500 Euclid Ave. Desk A100, Cleveland, OH 44195 Email: [email protected]

Warshaw, Andrew L., MD ACTIVE | 2014 Massachusetts General Hospital Administration Address: 55 Fruit St., BUL 370 Boston, MA 02114 Email: [email protected]

Watson, Chris, MD INACTIVE | 2010 Fox Chase Cancer Center Email: [email protected]

Weaver, Donald W., MD ACTIVE | 2014 Wayne State Univ. Dept. of Surgery Address: 3990 John R. Detroit, MI 48201 Email: [email protected]

Weber, Cynthia, MD RESIDENT | 2013 Loyola Univ. Medical Center Dept of Surgery Address: 2160 S First Ave. Maywood, IL 60153 Email: [email protected]

Weber, Sharon, MD ACTIVE | 2014 UW School of Medicine and Public Health Dept. of Surgery Address: 738 Oneida Place Madison, WI 53711 Email: [email protected]

Weiss, Matthew, MD INACTIVE | 2009 Johns Hopkins Hospital Email: [email protected]

Wellner, Ulrich, MD RESIDENT | 2014 UKSH Campus Lübeck Address: Ratzeburger Allee 160 Lübeck, 23562 Germany Email: [email protected]

147



Wey, Jane, MD ACTIVE | 2013 Cleveland Clinic General Surgery Address: 9500 Euclid Ave., #A100 Beachwood, OH 44122 Email: [email protected]

Whang, Edward, MD INACTIVE | 2011 Brigham & Women’s Hospital Email: [email protected]

White, Patrick, MD INACTIVE | 2011 Indiana Univ. School of Medicine Email: [email protected]

White, Rebekah, MD ACTIVE | 2013 Duke Univ. Surgery Address: DUMC Box 3247 Durham, NC 27710 Email: [email protected]

Wiatrek, Rebecca, MD INACTIVE | 2011 City of Hope Email: [email protected]

Wild, Aaron INACTIVE | 2012 Email: [email protected]

Williams, Sandra, MD INACTIVE | 2010 MD Anderson Cancer Center Email: [email protected]

Williard, Deborah, BSCHE INACTIVE | 2009 ICVAMC Univ. of Iowa Email: [email protected]

Wilson, Stuart, MD ACTIVE | 2014 Medical College of Wisconsin Dept. of Surgery Address: 9200 W. Wisconsin Ave. Milwaukee, WI 53226 Email: [email protected]

Windsor, John, MD INACTIVE | 2012 Univ. of Auckland Email: [email protected]

Winner, Megan INACTIVE | 2012 Email: [email protected]

Winslow, Emily R., MD ACTIVE | 2014 UW School of Medicine and Public Health Dept. of Surgery Address: 600 Highland Ave. K4/749 Madison, WI 53792 Email: [email protected]

Winter, Jordan M., MD ACTIVE | 2014 Thomas Jefferson Univ. Surgery Address: 1025 Walnut St., St. 605 College Philadelphia, PA 19107 Email: [email protected]

Witkowski, Elan, MD INACTIVE | 2012 UMass Medical School Email: [email protected]

Wolf, Andrea, MD ACTIVE | 2013 Spectrum Health Address: 145 Michigan St., NE Grand Rapids, MI 49503 Email: [email protected]

Wolf, Ron INACTIVE | 2012 Email: [email protected]

Wolfgang, Christopher, MD, PhD ACTIVE | 2014 Johns Hopkins Univ. Surgical Oncology Address: 600 N Wolfe Street, 685 Blalock Baltimore, MD 21287 Email: [email protected]

Wong, Joyce, MD ACTIVE | 2014 Penn State Milton S. Hershey Medical Center Surgery Address: 500 Univ. Dr., MC 11070 Hershey, PA 17033 Email: [email protected]




Wood, Thomas, MD RESIDENT | 2014 Florida Hospital Tampa Dept. of General Surgery Address: 3000 Medical Park Dr. Suite 310 Tampa, FL 33613 Email: [email protected]

Worhunsky, David, MD RESIDENT | 2013 Address: 300 Pasteur Drive, #H3591 Stanford, CA 94305 Email: [email protected]

Xourafas, Dimitrios INACTIVE | 2012 Email: [email protected]

Yamaguchi, Junpei INACTIVE | 2012 Massachusetts General Hospital Email: [email protected]

Yamaguchi, Koji, MD INACTIVE | 2011 Univ. of Occupational and Environmental Health Email: [email protected]

Yamanaka, Junichi, MD INACTIVE | 2010 Hyogo College of Medicine Email: [email protected]

Yamaue, Hiroki, MD, PhD ACTIVE | 2014 Wakayama Medical Univ. Second Dept. of Surgery Address: 811-1 Kimiidera Wakayama, Wakayama 641-8510 Japan Email: [email protected]

Yang, Anthony, MD INACTIVE | 2011 Seoul National Univ. Bundang Hospital Email: [email protected]

Yeboah, Edward Kwasi, BSc, MB, ChB, MRCS(Ire) INACTIVE | 2012 Royal Perth Hospital Email: [email protected]

Yeo, Charles, MD ACTIVE | 2014 Thomas Jefferson Univ. Dept. of Surgery Address: 1015 Walnut St., Suite 620 Curtis Philadelphia, PA 19107 Email: [email protected]

Yeo, Theresa, PhD ACTIVE | 2014 Thomas Jefferson Univ. Dept. of Surgery Address: 1015 Walnut St, Suite 605B College Bldg Philadelphia, PA 19107 Email: [email protected]

Yeo, Dannel, PhD ACTIVE | 2013 The Univ. of Melbourne Dept. of Surgery Address: Austin Health, Studley Rd Heidelberg, VIC 3084 Australia Email: [email protected]

Yoon, Yoo-Seok, MD, PhD ACTIVE | 2014 Seoul National Univ. Bundang Hospital Surgery Address: 82 Gumi-ro 173 Beon-gil, Bundang-gu Seongnam-si, South Korea Email: [email protected]

Yoshida, Koji, MD, PhD ACTIVE | 2013 Kawasaki Medical School Address: 577, Matsushima Kurashiki, Okayama 7000192 Japan Email: [email protected]

Yuan, Zuobiao, MD, PhD INACTIVE | 2009 Univ. of Iowa Email: [email protected]

Zani, Sabino INACTIVE | 2012 Email: [email protected]

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Zaydfudim, Victor, MD, MPH RESIDENT | 2014 Univ. of Virginia Health Systems Address: PO Box 800709 Charlottesville, VA 22903 Email: [email protected]

Zdon, Michael J., MD INACTIVE | 2009 The Chicago Medical School Email: [email protected]

Zea, Nicolas INACTIVE | 2012 Email: [email protected]

Zeh, Herbert, MD ACTIVE | 2014 UPMC UPMC Cancer Pavilion Address: 5150 Centre Ave., Suite 417 Pittsburgh, PA 15232 Email: [email protected]

Zenilman, Michael, MD ACTIVE | 2014 John Hopkins Univ. Address: 12009 Titan Way Potomac, MD 20854 Email: [email protected]

Zerbi, Alessandro, MD ACTIVE | 2014 Humanitas Mirasole SpA Address: Via manzoni 56, Rozzano Milano, 20089 Italy Email: [email protected]

Zheng, Lei, MD, PhD ACTIVE | 2014 Johns Hopkins Univ. School of Medicine Oncology and Surgery Address: 1650 Orleans St., CRB1, Rm. 488 Baltimore, MD 21042 Email: [email protected]

Zhiyun, He, MD INACTIVE | 2010 Univ. of Oklahoma HSC Email: [email protected]

Zhvitiashvili, Igor ACTIVE | 2013 SSMA General Surgery Address: Frunze St. 40 Smolensk, 214006 Russia Email: [email protected]

Ziegler, Kathryn, MD INACTIVE | 2011 Indiana Univ. Email: [email protected]

Zimmermann, Carolin INACTIVE | 2010 Univ. Hospital Dresden Email: [email protected]

Zinner, Michael, MD ACTIVE | 2014 Brigham & Women’s Hospital Dept. of Surgery Address: 75 Francis St.

Boston, MA 02115 EMAIL: [email protected]

Zuberi, Kashif, MD INACTIVE | 2009 Marshfield Clinic Email: [email protected]

Zureikat, Amer Harran, MD ACTIVE | 2014 Univ. of Pittsburgh Medical Center Address: 5150 Centre Ave., Suite 421 Pittsburgh, PA 15232 Email: [email protected]

Zyromski, Nicholas, MD ACTIVE | 2014 Indiana Univ. School of Medicine Dept. of Surgery Address: 545 Barnhill Dr., EH, 5TH FLR Indianapolis, IN 46202 Email: [email protected]


TABLE OF CONTENTSPast & Future Meetings

PAST & FUTURE MEETINGS

DATE & LOCATION HOST

2013 WDW Swan & Dolphin Hotel, Orlando, FL Pablo Arnoletti

2012 Hyatt Mission Bay, San Diego, CA Mark Talamini

2011 Chicago, IL Gerard Aranha, Mark Talamonti, David Bentrem

2010 New Orleans, LA

2009 Chicago, IL Gerard Aranha, Mark Talamonti, David Bentrem

2008 San Diego, CA Mark Talamini, Mike Bouvet

2007 Children’s Medical Center, Washington, DC Dana Anderson

2006 Los Angeles, CA Howard A. Reber

2005 Chicago, IL Gerard V. Aranha, Richard Bell

2004 New Orleans, LA Alton Ochsner

2003 Orlando, FL Michael Murr

2002 San Francisco, CA Kimberly Kirkwood

2001 Hilton Atlanta, Atlanta, GA Aaron Fink

2000 University of California, SD, San Diego, CA A.R. Moosa

1999 Peabody, Orlando, FL Michael M. Murr, James G. Norman

1998 LSU, Tulane, New Orleans, LA J. Patrick O’Leary, Elmo Cerise

1997 University Health Sciences, Bethesda, MD John W. Harmon

1996 Laurel Heights, UCSF, San Francisco, CA Sean Mulvihill

1995 University of California, SD, San Diego, CA A.R. Moosa

1994 Tulane University, New Orleans, LA Elmo Cerise, J. Patrick O’Leary

1993 Massachusettes General Hospital, Boston, MA Andrew Warshaw

SAVE THE DATE49th Annual Pancreas Club Meeting May 15-16, 2015 Washington DC

151

Past & Future Meetings

1992 University of California, SF, San Francisco, CA Carlos Pellegrini

1991 LSU, Tulane, New Orleans, LA Elmo Cerise, J. Patrick O’Leary

1990 University of Texas, San Antonio, TX Bradley Aust

1989 Washington Hilton Gregory Bulkley, Frances Milligan, John Cameron

1988 Tulane University, New Orleans, LA Elmo Cerise

1987 University of Illinois, Chicago, IL Phillip Donahue

1986 Ft. Miley VA, San Francisco, CA Carlos Pellegrini

1985 Mt. Sinai Hospital, New York, NY David Dreiling

1984 LSU Medical Center, New Orleans, LA Francis Nance

1983 Washington Hilton, Washington, DC Francis Milligan

1982 University of Chicago, Chicago, IL A.R. Moosa

1981 Alumni Hall, NYU, New York, NY John Ranson

1980 Salt Lake City, UT Frank Moody

1979 LSU Medical Center, New Orleans, LA Isadore Cohn

1978 Jockey Club, Las Vegas, NV Charles Frey

1977 Toronto, Canada Roger Keith

1976 Doral on the Ocean, Miami, FL Robert Zeppa

1975 Univiversity of Texas, San Antonio, TX Bradley Aust

1974 No Meeting


1972 University of California, SF, San Francisco, CA Englebert Dunphy

1971 Sheraton Hotel, Philadelphia, PA John Howard

1970 University of Chicago, Chicago, IL Edward Paloyan


1968 University of California, SF, San Francisco, CA Leon Goldman

1967 Philadelphia, PA John Howard

1966 Northwestern, Evanston, IL Marion Anderson

PAST & FUTURE MEETINGS


49th ANNUAL MEETINGOF THE PANCREAS CLUBMay 15-16, 2015 in Washington, DC

SAVE THE DATE

www.pancreasclub.com

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th Annual Meeting of the PANCREAS CLUB · Welcome to the 48th Annual Meeting of the Pancreas Club...

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