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    i

    A CLINICOPATHOLOGICAL STUDY OF

    GASTRIC CARCINOMA

    By

    Dr. ROMMEL. S,M.B.B.S

    Dissertation Submitted to the

    Rajiv Gandhi University of Health Sciences, Karnataka

    In partial fulfillment

    of the requirements for the degree of

    MASTER OF SURGERYin

    GENERAL SURGERYUnder the guidance of

    Prof. B. JAGADISHM.S.Professor and Unit Chief

    Department of Surgery

    MYSORE MEDICAL COLLEGE AND RESEARCH INSTITUTE,

    MYSORE

    APRIL 2011

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    ii

    RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES

    DECLARATION BY THE CANDIDATE

    I hereby declare that this dissertation entitled A CLINICOPATHOLOGICAL

    STUDY OF GASTRIC CARCINOMA is a bonafide and genuine research work

    carried out by me under the guidance of my Guide Prof. B. JAGADISH, MS.

    Department of General Surgery, and with Prof. Mudassir Azeez Khan, Department of

    Community Medicine and Prof. Nataraju G., Department of Pathology Mysore

    Medical College and Research Institute, Mysore as Co-Guides

    Date:

    Place: Mysore

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    iii

    CERTIFICATE BY THE GUIDE

    This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL

    STUDY OF GASTRIC CARCINOMA is a bonafide research work done by

    Dr. Rommel .S. in partial fulfillment of the requirement for the degree of Master of

    Surgery in General Surgery.

    Date:

    Place: Mysore

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    iv

    CERTIFICATE BY THE CO-GUIDES

    This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL

    STUDY OF GASTRIC CARCINOMA is a bonafide research work done by

    Dr. Rommel .S. in partial fulfillment of the requirement for the degree of Master of

    Surgery, General Surgery.

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    v

    ENDORSEMENT BY THE HEAD OF THE DEPARTMENT AND

    PRINCIPAL

    This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL

    STUDY OF GASTRIC CARCINOMA is a bonafide research work done by Dr.

    ROMMEL. S. under the guidance of Prof. B. JAGADISH, Professor of Surgery,

    Department of General Surgery, at K.R. Hospital attached to Mysore Medical College

    and Research Institute, Mysore.

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    vi

    COPYRIGHT

    Declaration of the candidate

    I hereby declare that The Rajiv Gandhi University of Health

    Sciences, Karnataka shall have the rights to preserve, use and

    disseminate this dissertation/ thesis in print or electronic format

    for academic/ research purpose.

    Rajiv Gandhi University of Health Sciences, Karnataka

    Date:

    Place: MysoreDr. ROMMEL. S

    Post Graduate in GeneralSurgery

    Mysore Medical Collegeand Research Institute,

    Mysore

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    vii

    ACKNOWLEDGEMENT

    It gives me great pleasure in preparing this dissertation and I take this opportunity to

    thank everyone who has made this possible. It is most appropriate that I begin by

    expressing my gratitude to the Almighty for his Blessings.

    I express my deep sense of gratitude and indebtedness to my most respected guide and

    treasured teacher Prof. B. Jagadish. M.S., Professor and Unit Chief, Department of

    Surgery, Mysore Medical College and Research Institute, Mysore whose wisdom and

    appropriate blend of science and art in the practice of surgery has been and will

    always be a constant source of encouragement.

    I express my deep sense of gratitude to my Co-guides, Prof. Mudassir Azeez Khan,

    Head of thye Department of Community Medicine and Prof. Nataraju G., Department

    of Pathology for their support and guidance throughout this study.

    I express my sincere thanks to Dr. AVADHANI GEETA. K., Professor and HOD of

    Surgery, MMC&RI Mysore for her valuable advice and support.

    I am also thankful to Assistant Professor Dr. Balasubrahmanya and Senior Resident

    Dr. B.G. Ponnappa for their constant support, encouragement and valuable

    suggestions.

    I thank all the staff of the Department of General Surgery for all the help rendered.

    I owe a lot to my post graduate colleagues and interns for their encouragement and

    enthusiastic co- operation.

    I always remember my family especially my brother for his support and

    encouragement.

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    viii

    I would like to thank Dr. Swati Kaktikar without whose help this would not have been

    possible.

    Lastly I would like to thank all the patients and their attenders for their co-operation.

    Date :

    Place : MysoreDr.ROMMEL. S

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    ix

    LIST OF ABBREVIATIONS USED

    (in alphabetical order)

    A-Ascites

    B- Body

    C- Cardia

    D-Diffuse

    DC- Decreased capacity

    DS- Dilated Stomach

    EL- Emergency Laparotomy

    EP- Enlarged Prostate

    F-Fundus

    FJ- Feeding Jejunostomy

    G- Growth

    GEJ- Gastro-oesophageal junction

    GC- Greater curvature

    HPR- Histopathology report

    I- Infiltrative

    IO- Inoperable

    JJ- Jejunojejunostomy

    LC- Lesser curvature

    LS- Liver secondaries

    M- Moderate

    MA Minimal Ascites

    MRD- Medical Renal Disease

    O- Operable

    P- Poor

    PA- Pyloric Antrum

    PALN- Paraaortic Lymph nodes

    PE- Pleural effusion

    Per- Perforation

    Po- Polypoidal

    PO- Pyloric Obstruction

    PG- Partial Gastrectomy

    PGJ- Palliative GJ

    PGLN- Perigastric Lymph Nodes

    PHLN- Porta Hepatis Lymph Nodes

    PR- Per rectal examination

    S-Splenomegaly

    SWT- Stomach wall thickening

    U-Ulcerative

    UGI- U er astrointestinal

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    x

    ABSTRACT

    Background

    Cancer is the second most common cause of cancer related deaths worldwide. Major

    changes have been noted in the site of gastric cancer occurrence. The west has noted a

    paradigm shift with a steady increase in cancers of the proximal stomach and a

    decline in cancers of the distal stomach. Gastric cancer is well known to be associated

    with risk factors

    Objectives

    This study was undertaken at K.R. Hospital, Mysore attached to Mysore Medical

    College and Research Centre to study the trends regarding prevalence, clinical

    features, association of risk factors, site of occurrence and histopathology.

    Methods

    All patients with histological confirmation of gastric carcinoma attending

    K.R.Hospital from January 2009 to July 2010 were studied and details regarding the

    clinical presentation, sub site, pathological features and treatment were collected.

    Results

    Thirty two patients with histological confirmation of carcinoma stomach were

    studied. Gastric carcinoma was seen in the older age group with male preponderance.

    The association of risk factors was studied. Majority of the patients presented in the

    advanced stage and distal tumours were the predominant subtype.

    Interpretation and Conclusion

    Gastric cancer is a common malignancy in this part and is commonly seen in the older

    age group predominantly in males. Patients usually present in the advanced stage,

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    however with the increasing use of upper gastrointestinal endoscopy early gastric

    cancers are also being detected.

    The association of risk factors is well known and consistent and hints at the

    primordial prevention of the disease.

    Unlike in the west where there has been a shift in the site of the tumour, distal

    tumours continue to be the major subtype in this study.

    A multidisciplinary approach combining population screening with molecular

    biological techniques that are being developed is required to detect the cancer early

    and improve prognosis.

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    xii

    TABLE OF CONTENTS

    SINo.

    Contents Pagenumber

    1 Introduction 1

    2 Objectives 9

    3 Review of Literature 5

    4 Methodology 56

    5 Results 58

    6 Discussion 79

    7 Conclusion 85

    8 Summary 87

    9 Bibliography 88

    10 Annexures 94

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    LIST OF TABLES

    Sl. No Tables Pages

    1 Lauren Classification System 12

    2 Genetic Abnormalities in Gastric Cancer 17

    3 TNM staging of gastric cancer 34

    4 Stage grouping gastric carcinoma 34

    5Japanese Gastric Cancer Association Staging System for

    Gastric Cancer

    36

    6Sex distribution among carcinoma stomach patients

    38

    7Age distribution among carcinoma stomach patients

    60

    8Income group among carcinoma stomach patients

    61

    9 Comparison of risk factors between males and females 62

    10Blood group distribution in carcinoma stomach patients 64

    11Symptom analysis in patients of carcinoma stomach 66

    12Analysis of signs in gastric cancer patients 68

    13Sub site specific trends in carcinoma stomach 70

    14Comparison of the macroscopic type in both sexes 71

    15Comparision of symptoms with the site of the tumour 72

    16Comparision of symptoms with macroscopic appearance 73

    17Analysis of the site of tumour with signs 74

    18Comparison of macroscopy with clinical signs 75

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    19Comparison of histopathology 76

    20Comparision of histology with the site of the tumour 77

    21 Sex distribution among carcinoma stomach patients 80

    22 Age distribution among carcinoma stomach patients80

    23Socioeconomic groups among gastric cancer patients 81

    24Blood group distribution in carcinoma stomach patients 81

    25 Comparison of risk factors between males and females82

    26Symptom analysis in patients of carcinoma stomach 83

    27Sub site specific trends in carcinoma stomach 83

    28Comparison of histology according to Broders classification 84

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    xv

    LIST OF FIGURES

    Sl.No Figures Pages

    1 Borrmann classification of gastric carcinoma 8

    2 Photomicrographs of gastric adenocarcinoma. 12

    3 Role of Helicobacter pylori 17

    4 T Stage defined by depth of penetration into gastric wall 34

    5 Lymph node station numbers as defined by Japanese Cancer

    Association 37

    6 Japanese classification system for early gastric cancer 41

    7 Endoscopic photograph showing ulceroproliferative growth in

    antrum98

    8 Endoscopic photograph showing early gastric cancer 98

    9 Photograph showing gastric cancer invading the posterior wall and

    perforating it99

    10 Photograph showing palliative anterior gastrojejunostomy 99

    11 Photograph showing partial gastrectomy specimen 100

    12 Photograph showing opened partial gastrectomy specimen 100

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    1

    INTRODUCTION

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    INTRODUCTION

    Adenocarcinoma of the stomach was the leading cause of cancer-related

    death worldwide through most of the 20th century. It now ranks second only to

    lung cancer, and an estimated 875,000 new cases are diagnosed annually

    worldwide. In many parts of the world, however, the incidence of gastric cancer

    has gradually decreased, principally because of changes in diet, food preparation,

    and other environmental factors. The declining incidence has been dramatic in the

    United States, where this disease ranks seventh as a cause of cancer-related deaths.

    Stomach cancer incidence rates are much lower in India than elsewhere, but the

    stomach remains one of the 10 leading sites of cancer in both sexes in most of the

    metropolitan registries. Cancer rates in India are rising with increasing migration

    of rural population to the cities, increase in life expectancy and changes in

    lifestyles.

    Change of diet is among the factors that may be responsible for the

    changing disease rates. Diet in India encompasses diversity unknown to most other

    countries, with many dietary patterns emanating from cultural and religious

    teachings that have existed for thousands of years. Very little is known, however,

    about the role of the Indian diet in causation of cancer or its role, if any, in

    prevention of cancer, although more attention is being focused on certain aspects

    of the Indian diet, such as vegetarianism, spices, and food additives.

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    The prognosis for this disease remains poor except in a few countries. The

    explanations for these poor results are multifactorial. The lack of defined risk

    factors and specific symptoms and the relatively low incidence have contributed to

    the late stage at diagnosis seen in most Western countries. In Japan, where gastric

    cancer is endemic, more patients are diagnosed at an early stage, which is reflected

    by higher overall survival rates.

    Although the incidence of gastric cancer has decreased dramatically over

    the past century, the decline has been limited to cancers below the esophagogastric

    junction. The number of newly diagnosed cases of proximal gastric and

    esophagogastric junction adenocarcinomas has increased markedly since the mid-

    1980s. These tumors are thought to be biologically more aggressive than distal

    tumors and more complex to treat.

    The only proven, potentially curative treatment for gastric cancer is

    surgical resection of all gross and microscopic disease. Even after what is felt to

    be a curative gastrectomy, disease recurs in both regional and/or distant sites in the

    majority of patients. Efforts to improve these poor results have focused on

    developing effective pre- and postoperative systemic and regional adjuvant

    therapies.

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    AIMS AND OBJECTIVES OF THE STUDY

    1. To study the prevalence of carcinoma stomach as occurring in K.R.Hospital ,

    Mysore.

    2. To study the clinical presentation including the anatomic site of occurrence and

    Histological type

    3. To study the association of risk factors

    4. To study the surgical modalities of treatment

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    REVIEW OF LITERATURE

    The stomach is a remarkable organ with important digestive, nutritional,

    and endocrine functions. The stomach stores and facilitates the digestion and

    absorption of ingested food, and it helps regulate appetite1. Wallace P. Ritchie, Jr.

    called the stomach an elegant organ, once thought to be the seat of the soul,

    always handy to bring to the dinner table, and a recognized source of ecstasy and

    grief2. Approximately 90% of all tumours of the stomach are malignant, the vast

    majority of which are adenocarcinoma.3

    EPIDEMIOLOGY

    Worldwide, gastric cancer remains the second or third most common

    malignancy (nearly 900,000 new cases annually) and the second most common

    cause of death (approximately 650,000 deaths).3, 4The incidence of gastric cancer

    has significant geographic variation, with the highest incidence (75 to 100 per

    100,000 men) occurring in Japan, Korea and parts of South America and Eastern

    Europe and the lowest incidence(as low as 5 per 100,000 men) occurring in the

    United States and Western Europe.3,5

    In India, the stomach was estimated to be the fifth leading site in males and

    the seventh in females in 1991 with age-standardized rates (ASRs) of 5.0 and 2.8

    per 100,000 in males and females, respectively.

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    With the establishment of the National Cancer Registry Programme, cancer

    incidence data are available for 5 metropolitan areas and 1 rural area in India since

    1982. From 1988 through 1992, the stomach was the leading site of cancer in

    males in Chennai (ASR = 15.9 per 100,000) and Bangalore (ASR = 10.3), fifth in

    Mumbai (ASR = 7.7) and fourth in Trivandrum (ASR = 6.8); among females, it

    was the fourth leading site in Chennai (ASR = 7.0), fifth in Bangalore (ASR = 5.1)

    and sixth in both Mumbai (ASR = 3.8) and Trivandrum (ASR = 2.5).6

    In contrast with the general decline in incidence, an increase has been

    observed for cardia lesions in many regions. Comparatively high rates are evident

    for the United Kingdom/Ireland, Northern Europe, Australia and New Zealand,

    China, and North America. The increase in incidence of cardia lesions has been

    associated with parallel increases for adenocarcinomas of the lower esophagus,

    where hyperacidity, reflux esophagitis, Barretts esophagus, and obesity have been

    proposed as likely risk factors. 7In a study conducted in Tamil Nadu, the sites of

    gastric cancer in order of frequency were antrum (67.3%) followed by

    body(23.3%), proximal stomach(5.6%) and OGJ(3.8%) .8 A recent study from the

    southern state of Kerala showed that carcinoma of the distal stomach has remained

    predominant although a trend towards a proximal shift has been noticed. 9

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    PATHOLOGY AND TUMOR BIOLOGY

    Approximately 95% of all malignant gastric neoplasms are

    adenocarcinomas, and in general, the term gastric cancer refers to adenocarcinoma

    of the stomach. Other malignant tumors are very rare and include squamous cell

    carcinoma, adenoacanthoma, carcinoid tumors, and leiomyosarcoma. Although no

    normal lymphoid tissue is found in the gastric mucosa, the stomach is the most

    common site for lymphomas of the gastrointestinal tract. 10

    Morphologic features and classification

    In 1965, Lauren described two histologic types of gastric adenocarcinoma,

    intestinal and diffuse, which provided a model to understand better the etiology

    and epidemiology of the disease.

    Several pathologic classifications have been proposed based on the

    morphologic features of gastric tumors.

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    The Borrmann classification divides gastric cancer into five types depending on

    macroscopic appearance.

    Type Irepresents polypoid or fungating cancers

    Type IIencompasses ulcerating lesions surrounded by elevated borders

    Type III represents ulcerated lesions infiltrating the gastric wall

    Type IVare diffusely infiltrating tumors

    Type Vare unclassifiable cancers10,11

    Fig. 1 Borrmann classification of gastric carcinoma

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    Gross Morphology

    There is wide variation in the gross appearance of carcinoma of stomach.

    Many intermediate stages exist between the two extremes represented by the

    fungating tumour growing mainly into the lumen and the flat, ulcerated and deeply

    invasive tumour growing through the wall of the stomach.

    Carcinomas located in the fundic area are more likely to have invaded the

    submucosa and beyond at the time of surgery than those located in the pyloric

    area.

    Depending upon the relative amounts of mucin secreted and desmoplastic

    reaction elicited, the tumour may have a fleshy, fibrous or gelatinous gross

    appearance. In terms of location, any area of the stomach can be affected: anterior

    and posterior wall, lesser curvature, and greater curvature (in that order of

    frequency). Multiple tumours are found in approximately 6% of cases.

    The non neoplastic mucosa adjacent to the carcinoma is often thickened; a

    feature that may result in false negative endoscopic biopsies and that has been

    attributed to production of epidermal growth factor by the tumour.

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    Microscopy

    Nearly all gastric carcinomas are of the adenocarcinoma type and

    composed of one or more of the following four major cell types- foveolar,

    mucopeptic, intestinal columnar and goblet cell.

    As, described by Lauren, two major categories exist, which have been designated

    intestinal (53%) and diffuse (33%).

    The intestinal type of sporadic gastric adenocarcinoma has a hallmark

    progression from normal gastric epithelium to atrophic to chronic atrophic gastritis

    (typically due to Helicobacter infection) to intestinal metaplasia to dysplasia to

    cancer. This assumption supported by electron microscopic and

    immunohistochemical studies.

    Their degree of differentiation ranges widely and correlates inversely with

    tumor size. In the better differentiated tumors, most of the cells are columnar and

    mucin secreting. Poorly differentiated variants have a predominantly solid pattern.

    Exceptionally the better differentiated tumors are ciliated. The amount of mucin

    production is highly variable, when abundant; it is often accompanied by

    calcification.

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    Diffuse type adenocarcinoma are best represented by the tumour type

    clinically known as linitus plastica and currently designated as signet ring (adeno)

    carcinoma. The gross alteration usually begins in the prepyloric area. Pyloric

    obstruction often develops, as the wall of the stomach becomes thickened and

    rigid. Sections of the wall show marked submucosal fibrosis, with or without

    mucosal ulceration. The muscle is hypertrophied and segmented by the presence

    of the parallel, grayish white, longitudinal lines that give it a comb like

    appearance. The lines are continuous with foci of subserosal thickening.

    Microscopically a diffuse growth of malignant cells is seen, associated with

    extensive fibrosis and inflammation. Often the entire wall is involved.

    Although an intramural type of signet ring carcinoma occurs in many cases

    of this entity the mucosa is less affected than the deeper layers. Glandular

    formations are rare and most tumour cells grow individually. Most of the mucin

    produced as intra-cytoplasmic, resulting in the typical signet ring appearance.

    There are few malignant tumours in the body that are more likely to be missed on

    microscopic examination than this type of gastric carcinoma. Over the years

    specimens have been seen from the stomach wall, lymph nodes, mesentery, pelvic

    peritoneum and ovary that were initially misinterpreted as a begin process because

    of the inconspicuousness of the tumour cell and the marked degree of

    inflammatory and desmoplastic reaction. The tumour may also simulate

    lymphoma because of its diffuse pattern of growth and the round shape of the cells

    and their nuclei. 11

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    Figure 2 Photomicrographs of gastric adenocarcinoma. A,Gastric adenocarcinoma intestinal

    type (H&E, 25). B,Gastric adenocarcinoma intestinal type (H&E, 400). C,Gastric

    adenocarcinoma diffuse type (H&E, 25). D,Gastric adenocarcinoma diffuse type (H&E,

    400).Arrowson signet ring cells.

    Table 1-- Lauren Classification System

    INTESTINAL DIFFUSE

    Environmental Familial

    Gastric Atrophy, metaplasia Blood group A

    Men>Women Women>men

    Increasing incidence with age Younger age group

    Gland formation Poorly differentiated, signet ring cells

    Hematogenous spread Transmural/lymphatic spreadMicrosatellite instability, APC gene

    mutations

    Decrease E-cadherin

    p53, p16 inactivation P53, p16 inactivation

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    Broder's classification of gastric cancer grades tumors histologically from 1

    (well-differentiated) to 4 (anaplastic). Bearzi and Ranaldi have correlated the

    degree of histologic differentiation with the gross appearance of 41 primary gastric

    cancers seen on endoscopy. Ninety percent of protruding or superficial cancers

    were well differentiated (Broder's grade 1), whereas almost half of all ulcerated

    tumors were poorly differentiated or diffusely infiltrating (Broder's grades 3 and

    4).8

    The WHO classification, 2000 classifies gastric cancer into

    Adenocarcinoma- intestinal and diffuse types,

    Papillary adenocarcinoma,

    Tubular adenocarcinoma,

    Mucinous adenocarcinoma,

    Signet ring cell adenocarcinoma,

    Adenosquamous adenocarcinoma,

    Squamous cell carcinoma,

    Small cell carcinoma,

    Undifferentiated carcinoma and Others.11,12

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    Classification of Esophagogastric Junction Cancers

    Siewert and Stein have developed a classification system for adenocarcinoma

    of the esophagogastric junction. Now commonly referred to as the Siewert

    classification, this system recognizes three distinct clinical entities that arise

    within 5 cm of the junction of the tubular esophagus and the stomach:

    Type 1: Adenocarcinoma of the distal esophagus, which usually arises

    from an area with specialized intestinal metaplasia of the esophagus (i.e.,

    Barrett's esophagus) and may infiltrate the esophagogastric junction from

    above.

    Type II: Adenocarcinoma of the cardia, which arises from the epithelium of

    the cardia or from short segments with intestinal metaplasia at the

    esophagogastric junction

    Type III: Adenocarcinoma of the subcardial stomach, which may infiltrate

    the esophagogastric junction or distal esophagus from below

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    The assignment of tumors to one of these subtypes is based on morphology

    and the anatomic location of the epicenter of the tumor. Classification can be

    performed based on the results of contrast radiography, endoscopy, CT, and

    operative findings. The Siewert classification has important therapeutic

    implications.13,14

    Histochemical, immunohistochemical and electron microscopic features

    The secretory product of most gastric adenocarcinoma(esp those of the

    intestinal type) is an acid mucosubstance, easily detected with Mayers

    mucicarmine, Alcian blue or colloidal iron stains and having feature analogous to

    the those of intestinal type mucins. Various alterations in the syalidation of the

    mucins occur and can be detected histochemically or immunohistochemically.

    At the immunohistochemical level, the main mucin types expressed are

    MUC1 for the intestinal type, MUC5AC for the diffuse and MUC2 for mucinous

    types. There is also an interesting relationship between mucin type and is

    prevalent with carcinoma of the antrum whereas MUC2 is expressed in greater

    amounts in carcinoma of the cardia.

    In terms of immunomarkers reactivity of gastric adenocarcinoma for

    keratin, epithelial membrane antigen and CEA is the rule.11

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    RISK FACTORS

    Inherited Susceptibility

    Case-control studies have observed consistent, up to threefold, increases in

    risk for gastric cancer among relatives of patients with gastric cancer. Studies of

    monozygotic twins have even shown a slight trend toward increased concordance

    of gastric cancers compared with dizygotic twins. Large families with an

    autosomal dominant, highly penetrant inherited predisposition for the development

    of gastric cancer are rare. However, early-onset diffuse gastric cancers have been

    described and linked to the E-cadherin/CDH1 locus on 16q and associated with

    mutations in this gene. This seminal finding has been confirmed in other studies

    with gastric cancers at a relatively high (67% to 83%) penetrant rate. Thus, E-

    cadherin mutation testing should be considered in the appropriate clinical setting.

    In fact, prophylactic gastrectomy should be considered strongly in families with

    germ line E-cadherin mutation even without gross mucosal abnormalities by

    endoscopic examination of the stomach.

    Hereditary nonpolyposis colon cancer (HNPCC) involves germ line

    mutations of DNA mismatch repair genes. Gastric adenocarcinoma may be

    observed in families with HNPCC. Gastric cancers have also been noted to occur

    in patients with familial adenomatous polyposis and Peutz-Jeghers syndromes.14

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    Table 2 - Genetic Abnormalities in Gastric Cancer

    Abnormalities Gene Approximate Frequency %

    Deletion/suppression p53 6070

    FHIT 60

    APC 50DCC 50

    E-cadherin

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    Role of helicobacter pylori

    As a commensal organism, Helicobacter pylori infection is widely

    prevalent throughout the world. Despite its classification by the World Health

    Organization as a class I carcinogen, infection with H. pylori does not typically

    lead to gastric cancer. This underscores the importance of other factors, such as

    virulence, environmental, and host factors, as well as genetic polymorphisms (e.g.,

    in interleukin-1, a potent inhibitor of acid secretion). The blood group A

    phenotype has been reported to be associated with gastric cancers. Helicobacter

    pylori may adhere to the Lewis Blood Group antigen, indicating a factor for

    increased risk for gastric cancer. Small variant alleles of a mucin gene, Muc1,

    were found to be associated with gastric cancer patients when compared with a

    blood donor control population.

    The risk of gastric cancer in patients with chronic H. pylori infection is

    increased about threefold. When compared to uninfected patients, patients with a

    history of gastric ulcer are more likely to develop gastric cancer , and patients with

    a history of duodenal ulcer are at decreased risk for gastric cancer. This may be

    due to the fact that some patients develop antral-predominant disease

    (predisposing to duodenal ulcer and somehow protecting against gastric cancer),

    while other patients develop corpus-predominant gastritis, resulting in

    hypochlorhydria and somehow predisposing to gastric ulcer and gastric cancer.

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    Recently, it has been demonstrated that bone marrowderived stem cells

    play a key role in the pathogenesis of gastric adenocarcinoma in patients with

    chronic H. pylori infection. However, it must be recognized that gastric

    adenocarcinoma is a multifactorial disease. Not all patients with gastric cancer

    have H. pylori, and there are some geographic areas with a high prevalence of

    chronic H. pylori infection and a low prevalence of gastric cancer (the "African

    enigma"). Finally,H. pyloriinfected patients seem to be at decreased risk for the

    development of adenocarcinoma of the distal esophagus and cardia region.

    Perhaps the corporeal gastritis decreases acid secretion, creating a less damaging

    refluxate and thus reducing the risk for Barrett's esophagus, the precursor lesion

    for these tumors.14

    Epstein Barr Virus

    Epstein-Barr virus (EBV) has been found to be associated with a type of

    gastric carcinoma (EBVaGC). EBV may be a factor initiating EBVaGC. EBV may

    infect the surface epithelium of the stomach through the reactivated EBV-carrying

    lymphocytes. Using PCR and EBER1 in situ hybridization, EBVaGC (definitely

    amplifiable EBV-DNA and positive EBER1-signal in the nuclei of carcinoma

    cells) was found in 8 of 72 gastric carcinomas (11%). EBVaGC was found in the

    cardia (4/8) or body (4/8) of the stomach, and consisted of 7 advanced and 1

    intramucosal carcinoma.

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    Patients with EBVaGC showed high titers of anti-VCA IgG (8/8), anti-

    VCA IgA (2/8) and anti-EA IgG (7/8) antibodies just before surgery. Anti-EBV

    antibodies or EBER1 in situ hybridization may help to identify patients at high

    risk for EBVaGC stomach.15

    Diet

    Diet is generally accepted as the main factor in gastric cancer etiology.

    There is, however, no general agreement on the specific components of the diet

    supposedly responsible for gastric cancer. The geographic distribution of the

    disease shows marked inter-country contrasts but there are many examples of

    culturally-divergent populations inhabiting the same land but having contrasting

    gastric cancer rates. Migrants from high-risk areas acquire the low rates of

    adoptive countries. Culture, not race or geography, appears as the main

    determinant of gastric-cancer risk. Diet is the cultural component which offers the

    most logical explanation of inter-population contrasts.

    The gastric-cancer diet has been characterized as follows

    (a) Low in animal fat and animal proteins

    (b) High in complex carbohydrates

    (c) A substantial proportion of the protein obtained from vegetable sources,

    mostly grains and tubers

    (d) Low in salads and fresh, green, leafy vegetables

    (e) Low in fresh fruits, especially citrus

    (f)

    High in salt.

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    In addition, a controversial role of nitrates has been reported.16Nitrates are

    converted to carcinogenic nitrites by bacteria. Such bacteria may be introduced

    through consumption of partially decayed foods, a practice that is more common

    in the lower social economic strata worldwide.2

    Humans are exposed to a wide range of N-nitrosocompounds (NOCs) from

    diet, tobacco smoking, work place and drinking water, which are the major source

    of exposure in the general population. Preformed exogenous nitrosamines are

    found mainly in cured meat products, smoked preserved foods, foods subjected to

    drying by additives such as malt in the production of beer and whiskey, pickled

    and salty preserved foods.

    Available data suggest that nitrosamines are found more frequently and at

    higher concentration in Asian foods than in Western foods. On the other hand,

    nitrosamines are formed endogenously from nitrate and nitrite. Although the levels

    have reduced during the last 20 years, sodium nitrites are still widely used as food

    preservatives in cured meat products. Nitrite is also formed in the human body

    from oral reduction of salivary nitrate. Vegetables and water are the main sources

    of nitrate intake. Nitrites are transformed into nitric oxide by gastric acid-catalyzed

    formation, which acts as nitrosating agent of amines and amides, as consequence

    of NOC. Under chronic inflammatory conditions, such as precancerous conditions

    of gastric cancer (GC) and esophageal cancer (OC), nitrosating agents are

    overproduced.17

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    Excessive salt intake as a factor has epidemiologic and experimental

    support.16A recent case-control study in Mumbai found that consumption of dried

    fish increased the risk while green tea consumption decreased the risk of having

    stomach cancer. A prospective case-control study from Trivandrum evaluated

    dietary risk factors for stomach cancer and found that high consumption of rice,

    spicy food, chili , and high-temperature food increased the risk of developing

    stomach cancer.

    Fried foods are associated with higher rates of cancer due in part to the

    production of carcinogenic or mutagenic heterocyclic amines (HA) during the

    cooking process. Case-control and prospective studies have reported an increased

    risk of stomach, colon, and bladder cancers with moderate to heavy consumption

    of fried foods. The use of the spice turmeric is associated with a reduced risk of

    stomach cancer, in part because of its protective effect against the carcinogenic

    bacterium H. pylori, a major risk factor for stomach cancer.18

    Conversely, the consumption of raw vegetables, citrus fruits, and high-fiber

    breads is associated with a lower risk for gastric cancer. The ascorbic acid and -

    carotene found in fruits and vegetables act as antioxidants, whereas ascorbic acid

    can also prevent the conversion of nitrates to nitrites.2

    In a carefully conducted case-control study at Chennai, the authors have

    identified alcohol consumption as an independent risk factor.19

    Studies of the

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    relation between alcohol consumption and the risk of GCA have been largely

    inconclusive, and case-control studies from India have not identified alcohol

    intake as an independent risk factor for GCA in India.20Beer specimens obtained

    from several Indian cities in South India have been shown to contain N-

    nitrosodimethylamine in large amounts,21and this may be an important factor for

    the high risk of GCA associated with alcohol consumption in our part of the

    country. 19

    PRECANCEROUS LESIONS

    Atrophic gastritis

    This is a histological diagnosis. The main features are a variable degree of

    inflammation, atrophy of gastric glands, and often associated intestinal metaplasia,

    which changes are more commonly found in the antrum than in the body or the

    fundus of the stomach.

    Patients with atrophic gastritis are statistically at increased risk from cancer

    of the stomach but precise measurement of this risk is yet to be determined. There

    is a significant geographical relationship between areas of high frequency for

    gastric carcinoma and the incidence of atrophic gastritis and intestinal metaplasia.

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    Within the histological spectrum of atrophic gastritis intestinal metaplasia

    is the most sensitive risk indicator. Most gastric cancers develop on a basis of

    atrophic gastritis, but the epithelial change which statistically most predisposes to

    malignancy is intestinal metaplasia.

    Gastric ulcer

    The incidence of so-called 'ulcer-cancer', that is, carcinoma developing in a

    pre-existing peptic ulcer, has been debated hotly for many years. There are two

    essential criteria for the diagnosis: first, there must be definite evidence of a pre-

    existing ulcer (complete destruction of a zone of muscle, dense fibrous tissue in

    the floor of the lesion, endarteritis and thrombophlebitis in surrounding vessels,

    fusion of muscle coats and muscularis mucosae at the edge of the lesion) and,

    second, there must be definite evidence of malignant change at the edge of the

    ulcer quite distinct from any attempt at epithelial regeneration.

    In any assessment one must remember that chronic ulcer and cancer may

    coexist in a stomach without necessarily being causally related; studies in Japan

    suggest that gastric ulcer and gastric cancer also have a different geographic

    distribution. Ulcer-cancers undoubtedly do occur, particularly when the ulcer is

    chronic, but the incidence of cancer developing in a proven peptic ulcer and the

    presence of unequivocal evidence of previous peptic ulcer at the site of a proven

    carcinoma are both probably not more than 1 %.

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    Pernicious anemia

    There is statistical and histological evidence that patients with pernicious

    anemia are at increased risk from cancer of the stomach. True adenomatous polyps

    and carcinoma of the stomach have been reported to be three to four times more

    common in patients with pernicious anemia than in the general population

    although a recent study suggests that this may be an underestimate, since some

    patients with carcinoma but without overt pernicious anemia are in a 'pre-

    pernicious anemia stage'.

    Moreover, it appears that the carcinomas are mostly found in the body or

    the fundus of the stomach rather than in the pyloric antrum, which is where most

    gastric cancers are seen. 22

    Gastric stumps

    Balfour first reported a correlation between prior gastric surgery for benign

    disease and the subsequent development of gastric cancer in 1922. Subsequent

    meta-analyses support the conclusion that there is an increased risk for gastric

    remnant cancer in patients with prior partial gastrectomy.However, the risk is only

    observed after a latency of 15 years and is increased in patients operated on for

    gastric but not duodenal ulcers.

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    The incidence of malignancy ranges from 2% to 6% in gastric remnants,

    and a variety of causative factors have been proposed to include alkaline duodenal

    gastric reflux as well as increased N-nitroso compounds secondary to bacterial

    overgrowth. The development of atrophic gastritis along with gastritis cystica

    profunda can be associated with dysplasia in 5% of patients, for which

    surveillance endoscopy is indicated.2

    Gastric stump carcinomas usually develop close to the anastomosis on the

    gastric side. Polypoid lesions are common in the same area, but their significance

    has not yet been established; many are hyperplastic or regenerative polyps, and

    others may be pseudo polyps resulting from the construction of the anastomosis.22

    Gastric polyps

    Polypoid lesions of the stomach can be divided into those with and without

    malignant potential. The common ones, hyperplastic or regenerative polyps, have

    insignificant malignant potential. Polypoid lesions in which the epithelium shows

    dysplasia (which are called adenomas or borderline lesions by some) have a

    significant capacity for malignant change. It is exceptional for gastric adenomas to

    have a stalk, particularly a long one, and most of them are sessile. They can be

    very flat, slightly elevated tumours and are more often single than multiple.

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    Most gastric adenomas are of the intestinal type, which suggests that they

    have developed on a basis of atrophic gastritis and intestinal metaplasia. Gastric

    adenomas are uncommon but have a very significant potential for malignant

    change.

    It is possible that only a small minority of gastric cancers arise from

    previously benign adenomas. The diagnosis of benign adenoma must be made

    with care, because multiple sections through the tumour may show signs of

    intramucosal carcinoma.

    Mentriers Disease

    There is a growing list of case reports of carcinoma of the stomach

    complicating Menetrier's disease. The statistical risk of cancer in this disease is not

    known, and anyway the diagnosis of Menetrier's disease is difficult to define both

    clinically and pathologically.

    There are descriptions of both intestinal metaplasia and epithelial dysplasia

    of gastric epithelium in some of the reports.22

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    CLINICAL MANIFESTATIONS

    Most patients who are diagnosed with gastric cancer in the United States

    have advanced stage III or IV disease at the time of diagnosis. The most common

    symptoms are weight loss and decreased food intake due to anorexia and early

    satiety. Abdominal pain (usually not severe and often ignored) also is common.

    Other symptoms include nausea, vomiting, and bloating. Acute GI bleeding is

    somewhat unusual (5%), but chronic occult blood loss is common and manifests

    as iron deficiency anemia and heme-positive stool. Dysphagia is common if the

    tumor involves the cardia of the stomach. Paraneoplastic syndromes such as

    Trousseau's syndrome (thrombophlebitis), acanthosis nigricans

    (hyperpigmentation of the axilla and groin), or peripheral neuropathy are rarely

    present.

    Physical examination usually is normal. Other than signs of weight loss,

    specific physical findings usually indicate incurability. A focused examination in a

    patient in whom gastric cancer is a likely part of the differential diagnosis should

    include an examination of the neck, chest, abdomen, rectum, and pelvis. Cervical,

    supraclavicular (on the left referred to as Virchow's node), and axillary lymph

    nodes may be enlarged, and today can be sampled in the office with fine-needle

    aspiration cytology. There may be a metastatic pleural effusion, or aspiration

    pneumonitis in a patient with vomiting and/or obstruction.

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    An abdominal mass could indicate a large (usually T4 incurable) primary

    tumor, liver metastases, or carcinomatosis (including Krukenberg's tumor of the

    ovary). A palpable umbilical nodule (Sister Joseph's nodule) is pathognomonic of

    advanced disease, or there may be evidence on exam of malignant ascites.1

    Gastric carcinoma may also present as multiple cutaneous nodules.23

    Rectal exam may reveal heme-positive stool and hard nodularity

    extraluminally and anteriorly, indicating so-called drop metastases, or rectal shelf

    of Blumer in the pouch of Douglas.1

    Preoperative Evaluation

    Radiologic examination of the stomach can identify advanced gastric

    cancers; however it is less accurate than endoscopy for identification of early

    gastric cancer. All ulcers identified by x-ray examination should be referred for

    endoscopic biopsy.

    Radiologic criteria that suggest a benign ulcer include radiating folds and a

    normal-appearing mucosal surface around the crater. Linitus plastica is suggested

    by radiologic studies that demonstrate a nondistensible stomach.

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    Endoscopy

    When gastric cancer is suspected based on history and physical

    examination, flexible upper endoscopy is the diagnostic modality of choice.

    Although double-contrast barium upper GI radiography is cost-effective with 90%

    diagnostic accuracy, the inability to distinguish benign from malignant gastric

    ulcers makes endoscopy preferable. During endoscopy, multiple biopsy samples

    (seven or more) should be obtained around the ulcer crater to facilitate histologic

    diagnosis. When multiple biopsy specimens are taken, the diagnostic accuracy of

    the procedure approaches 98%.

    The addition of direct brush cytology to multiple biopsy specimens may

    increase the diagnostic accuracy of the study. Additionally, the size, location, and

    morphology of the tumor should be noted and other mucosal abnormalities

    carefully evaluated. In select patients with advanced disease,

    esophagogastroduodenoscopy provides a means for palliation through the use of

    laser ablation, dilation, or tumor stenting. Although not included in the National

    Comprehensive Cancer Network guidelines for the evaluation of gastric

    adenocarcinoma, some centers are using endoscopic Ultrasonography (EUS) to

    assist in the staging of this disease. EUS can gauge the extent of gastric wall

    invasion as well as evaluate local nodal status. However, EUS cannot reliably

    distinguish tumor from fibrosis; therefore, it is not a good modality for evaluating

    response to therapy.2

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    CT scan

    Computed tomography (CT) scans of the chest and abdomen are the

    primary imaging modalities for preoperative staging of stomach. In stomachs that

    are well distended with contrast, wall thickness of >2 cm indicates transmural

    extension of the tumor. Evidence of direct invasion of perigastric fat, diaphragm,

    pancreas, transverse colon, and left lobe of the liver should be sought. Metastases

    to the liver, lung, and other organs can also be documented.

    For gastric adenocarcinoma overall accuracy of preoperative CT scans

    ranges from 61 to 72%. 23 In women, a pelvic CT scan or ultrasound is also

    recommended. CT of the chest may be needed for proximal gastric cancers The

    major limitations of CT are in the evaluation of early gastric primaries and in the

    detection of small (

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    Positron Emission Tomography

    Whole-body PET scanning uses the principle that tumor cells preferentially

    accumulate positron-emitting 18F-fluorodeoxyglucose. This modality is most

    useful in the evaluation of distant metastasis in gastric cancer but can also be

    useful in locoregional staging. PET scan is most useful when combined with spiral

    CT (PET-CT) and should be considered before major surgery in patients with

    particularly high-risk tumors or multiple medical comorbidities.23

    Laparoscopy

    Because of the inaccuracy of CT and other modalities for the detection of

    macrometastases smaller than 5 mm on the peritoneal surface or liver, laparoscopy

    is recommended as the next step in the evaluation of patients with locoregional

    disease. Laparoscopy can detect metastatic disease in 23% to 37% of patients

    judged to be eligible for potentially curative resection by current-generation CT

    scanning.

    Laparoscopy may therefore improve palliation by avoiding a

    nontherapeutic laparotomy in patients presumed to have localized gastric cancer.

    The addition of laparoscopic ultrasonography may increase the sensitivity of

    laparoscopic staging in gastric cancer as it has in other abdominal malignancies.

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    Cytologic analysis of peritoneal fluid or of fluid obtained by peritoneal

    lavage may reveal the presence of free intraperitoneal gastric cancer cells,

    identifying patients with otherwise occult carcinomatosis. More sensitive methods

    of detecting free intraperitoneal gastric cancer cells, such as immunostaining and

    reverse-transcriptase polymerase chain reaction for carcinoembryonic antigen

    (CEA) messenger RNA, are under investigation.2

    STAGING

    Many staging systems have been proposed for gastric adenocarcinoma. A

    basic understanding of the older systems is necessary to understand the literature.

    The pathologic staging system currently in use worldwide is the AJCC TNM

    staging system. The TNM system can adequately stratify patients into distinct

    groups with different risks for tumor-related death. A major revision occurred in

    the AJCC staging system for gastric cancer in 1997 when nodal status

    stratification was changed from location of nodes to number of positive nodes. In

    the current staging system, a minimum of 15 nodes must be evaluated for accurate

    staging. Nodal staging is then determined by the number of positive nodes, with

    pN1 reflecting 1 to 6 positive nodes, pN2 designating 7 to 15 positive nodes, and

    pN3 more than 15 positive nodes. 2

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    TNM STAGING OF GASTRIC CARCINOMA

    Table 3TNM staging of gastric carcinoma

    Table 4: Staging of gastric carcinoma Fig .4 T Stage defined by depthof penetration into gastric wall

    T: Primary tumor

    Tis Carcinoma in situ; intraepithelial tumor without invasion of lamina propriaT1 Tumor invades lamina propria or submucosaT2 Tumor invades muscularis propria or subserosaT3 Tumor penetrates serosa (visceral peritoneum) without invasion of adjacent

    structuresT4 Tumor invades adjacent structures

    N: Regional lymph node

    N0 No regional lymph node metastasisN1 Metastasis in 1 to 6 regional lymph nodesN2 Metastasis in 7 to 15 lymph nodes

    N3 Metastasis in more than 15 regional lymph nodesM: Distant metastasisM0 No distant metastasisM1 Distant metastasis

    STAGE T N M

    0 Tis N0 M0IA T1 N0 M0IB T1 N1 M0

    T2 N0 M0II T1 N2 M0

    T2 N1 M0T3 N0 M0

    IIIA T2 N2 M0T3 N1 M0T4 N0 M0

    IIIB T3 N2 M0

    IV T4 N1-3 M0T1-3 N3 M0Any T Any N M1

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    Resection classification

    The termR statuswas first described by Hermanek in 1994 and is used to

    describe the tumor status after resection. R0 describes a microscopically margin-

    negative resection, in which no gross or microscopic tumor remains in the tumor

    bed. R1 indicates removal of all macroscopic disease, but microscopic margins are

    positive for tumor. R2 indicates gross residual disease. Because the extent of

    resection can influence survival, some authors include this R designation to

    complement the TNM system. Long-term survival can be expected only after an

    R0 resection; therefore, a significant effort should be made to avoid R1 or R2

    resections.

    Knowledge of the older staging systems and the Japanese system is crucial

    to the understanding of the debate regarding lymphadenectomies for gastric

    cancer. The Japanese Classification for Gastric Carcinoma (JCGC) staging system

    was designed to describe the anatomic locations of nodes removed during

    gastrectomy. Sixteen distinct anatomic locations of lymph nodes are described ,

    with the recommendation for nodal basin dissection dependent on the location of

    the primary. The lymph node stations or echelons are numbered and then further

    classified into groups of echelons that correspond to the location of the primary

    and reflect the likelihood of harboring metastases . The presence of metastasis to

    each lymph node group then determines the N classification. For example,

    metastases to any of the group 1 lymph nodes in the absence of disease in more

    distant lymph node groups is classified as N1. 2

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    Table 5 Japanese Gastric Cancer Association Staging System for Gastric Cancer

    TUMOR STAGET1 Tumor invasion of mucosa and/or muscularis mucosa (M) or submucosa (SM)T2 Tumor invasion of muscularis propria (MP) or subserosa (SS)

    T3 Tumor penetration of serosal (SE)T4 Tumor invasion of adjacent structures (SI)TX UnknownNODAL STAGE

    N0 No evidence of lymph node metastasisN1 Metastasis to group 1 lymph nodes, but no metastasis to groups 2 to 3 lymph

    nodesN2 Metastasis to group 2 lymph nodes, but no metastasis to group 3 lymph nodesN3 Metastasis to group 3 lymph nodesNX Unknown

    HEPATIC METASTASIS STAGE (H)H0 No liver metastasisH1 Liver metastasisHX UnknownPERITONEAL METASTASIS STAGE (P)P0 No peritoneal metastasisP1 Peritoneal metastasisPX UnknownPERITONEAL CYTOLOGY STAGE (CY)CY0 Benign/indeterminate cells on peritoneal cytologyaCY1 Cancer cells on peritoneal cytology

    CYXPeritoneal cytology was not performedOTHER DISTANT METASTASIS (M)M0 No other distant metastases (although peritoneal, liver, or cytological metastases

    may be present)M1 Distant metastases other than the peritoneal, liver, or cytological metastasesMX UnknownSTAGE GROUPING

    N0 N1 N2 N3T1 IA IB IIT2 IB II IIIA

    T3 II IIIA IIIB IVT4 IIIA IIIBH1, P1, CY1, M1aCytology felt to be suspicious for malignancy should be classified as CY0.

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    Fig 5 Lymph node station numbers as defined by Japanese Cancer Association

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    LOCATION OF PRIAMRY TUMOUR INTHE STOMACH

    LYMPH NODE STATION(No) DESCRIPTION Upper third Middle third Lower third

    1 Right paracardial 1 1 2

    2 Left paracardial 1 3 M

    3 Lesser curvature 1 1 1

    4sa Short gastric 1 3 M

    4sb Left gastroepiploic 1 1 3

    4d Right gastroepiploic 2 1 1

    5 Suprapyloric 3 1 1

    6 Infrapyloric 3 1 1

    7 Left gastric artery 2 2 2

    8a Anterior comm. hepatic 2 2 2

    8p Posterior comm. hepatic 3 3 3

    9 Celiac artery 2 2 2

    10 Splenic hilum 2 3 M

    11p Proximal splenic 2 2 2

    11d Distal splenic 2 3 M

    12a Left hepatoduodenal 3 2 2

    12b,p Posterior hepatoduodenal 3 3 3

    13 Retropancreatic M 3 3

    14v Superior mesenteric vein M 3 2

    14a Superior mesenteric artery M M M

    15 Middle colic M M M

    16al Aortic hiatus 3 M M

    16a2,b1 Para-aortic, middle M 3 3

    16b2 Para-aortic, caudal M M M

    M, lymph nodes regarded as distant metastasis

    Table 6- Grouping of Regional Lymph Nodes (Groups 1-3) by Location of Primary

    Tumor According to the Japanese Classification of Gastric Carcinoma

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    Spread of carcinoma of the stomach

    No better example of the various modes by which carcinoma spreads can

    be given than the case of stomach cancer. It is important to note that this distant

    spread is unusual before the disease spreads locally and distant metastases are

    uncommon in the absence of lymph node metastases. The intestinal and diffuse

    types of gastric cancer spread differently. The diffuse type spreads via the

    submucosal and subserosal lymphatic plexus and it penetrates the gastric wall at

    an early stage.

    Direct spread

    The tumour penetrates the muscularis, serosa and ultimately adjacent

    organs such as the pancreas, colon and liver.

    Lymphatic spread

    This is both by permeation and emboli to the affected tiers (see below) of

    nodes. This may be extensive, the tumour even appearing in the supraclavicular

    nodes (Trosiers sign). Unlike malignancies such as breast cancer, nodal

    involvement does not imply systemic dissemination.

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    Blood-borne metastases

    This occurs first to the liver and subsequently to other organs including

    lung and bone. This is uncommon in the absence of extensive nodal disease.

    Trans peritoneal spread

    This is a common mode of spread once the tumour has reached the serosa

    of the stomach and indicates incurability. Tumours can manifest anywhere in the

    peritoneal cavity and commonly give rise to ascites. Advanced peritoneal disease

    may be palpated either abdominally or rectally as a tumour shelf.

    The ovaries may sometimes may be the sole site of transcoelomic spread

    (Krukenbergs tumours). Tumour may spread via the abdominal cavity to the

    umbilicus (Sister Josephs nodule). 25

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    TREATMENT OF LOCALIZED DISEASE

    STAGE I DISEASE (EARLY GASTRIC CANCER) Classification and Risk

    for Nodal Metastases

    The Japanese Research Society for Gastric Cancer has classified early

    gastric cancers (EGC) based on endoscopic criteria first established by the

    Japanese Endoscopy Society for the description of T1 tumors.

    The current classification system is used for both in situ and invasive

    tumors and categorizes tumors based on endoscopic findings as follows:

    Figure 6 .Japanese classification system for early gastric cancer. In the combinedsuperficial types, the type occupying the largest area should be described first,followed by the next type (e.g., IIc + III). Type 0I and Type 0IIa are distinguished asfollows: Type 0I: The lesion has a thickness of more than twice that of the normalmucosa. Type 0IIa: The lesion has a thickness up to twice that of the normal mucosa.

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    Considering the risk for lymph node metastasis is important when

    evaluating treatment options for patients with EGC. The frequency and anatomic

    distribution of nodal disease are related to the depth of tumor invasion. 10

    Treatment options for patients with EGC include

    - Endoscopic Mucosal Resection (EMR),

    - Limited surgical resection,

    - Gastrectomy.

    Endoscopic Mucosal Resection

    This approach involves the submucosal injection of fluid to elevate the

    lesion and facilitate complete mucosal resection under endoscopic guidance. Only

    patients with tumors that have extremely low metastatic potential should be

    offered EMR.

    These are generally well-differentiated, superficial type IIa or IIc lesions

    smaller than 3 cm in diameter and located in an easily manipulated area. Tumors

    invading the submucosa are at increased risk for metastasizing to lymph nodes and

    are not usually considered candidates for EMR.

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    Limited Surgical Resection

    Given the low rate of nodal involvement for patients with EGC, limited

    resection may be a reasonable alternative to gastrectomy for some patients with

    early EGC. There are no well-accepted pretreatment criteria for selection of

    patients for limited resection. Based on the existing pathology data, patients with

    small (less than 3 cm) intramucosal tumors and those with nonulcerated

    intramucosal tumors of any size may be candidates for EMR or limited resection.

    Surgical options for these patients may include gastrectomy with local excision.

    Gastrectomy

    Gastrectomy with lymph node dissection should be considered for patients

    with EGC who cannot be treated with EMR or limited surgical resection and/or

    patients who have intramucosal tumors with poor histologic differentiation or size

    greater than 3 cm or who have tumor penetration into the submucosa or beyond.

    Gastrectomy with lymph node dissection allows for adequate pathologic staging

    and local therapy for these higher-risk patients.

    There is no consensus on the extent of lymphadenectomy that should be

    performed as part of gastrectomy for EGC. Dissection of level I lymph nodes is a

    reasonable minimum standard at this time.

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    STAGE II AND STAGE III DISEASE

    Surgery

    Surgical resection is the cornerstone of treatment for patients with localized

    gastric cancer. However, for stages II and III disease, surgery is necessary but

    often not sufficient for cure. The general therapeutic goal is to achieve a micro-

    and macroscopically complete resection (R0). 10

    Extent of Gastric Resection

    There is no evidence that an extended gastric resection above and beyond

    complete clearance of the primary tumor improves survival; i.e., total gastrectomy

    does not improve survival over distal or proximal gastrectomy, provided that thetumor is removed completely with negative transection margins (R0 resection).

    This has been confirmed in a number of randomized trials. The extent of

    the gastrectomy therefore is site-dependent and focuses on complete removal of

    the gastric carcinoma with preferably a 4- to 5-cm margin from the gross edge of

    the tumor. Clearly, anatomic limitations influence this margin because in antral

    lesions close to or involving the pylorus, only a limited portion of the duodenum

    can be removed.

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    In similar fashion, a lesser extent of uninvolved esophageal margin may be

    acceptable provided complete histologic resection is possible.

    In patients with a distal lesion, a distal subtotal gastrectomy is performed

    essentially regardless of T stage. For proximal gastric cancers and true GE

    junction cancers (Siewert types II and III), sub diaphragmatic proximal

    gastrectomy with esophagogastrectomy, can be liberally used whereas some prefer

    total gastrectomy for any lesion not in the antrum.

    For midbody or more extensive lesions, total gastrectomy is required,

    whereas for more distal lesions, a subtotal gastrectomy is the preferred approach.

    It is important to emphasize that in most studies there is an increase in morbidity

    and mortality when total gastrectomy is performed over distal subtotal

    gastrectomy. Since long-term survival is not improved by the more extensive

    resection, this is a further factor in favor of subtotal resection, provided that an R0

    resection can be obtained.

    Proximal resections, however, appear to have similar perioperative

    morbidity and mortality to total gastrectomy.

    Extended organ resection is reserved for patients with apparently node-

    negative T4 lesions, in which complete resection requires resection of the invaded

    portions of the diaphragm, pancreas, spleen, adrenal gland, or colon.27

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    Extent of Lymphadenectomy

    The dialogue surrounding lymphadenectomy involves at least two

    important issues: (1) staging removal and histopathologic analysis of an adequate

    number of lymph nodes, and (2) therapy determining if some forms of

    lymphadenectomy are therapeutic for patients with gastric cancer.

    The current AJCC staging system (sixth edition) requires analysis of 16 or more

    lymph nodes to assign a pathologic N stage.

    Adjuvant Therapy

    The term adjuvant therapy is best used to describe additional treatment in

    an attempt to increase cure rates in patients who have already undergone a

    potentially curative resection. For gastric cancer, an R0 surgical procedure, in

    which all gross disease has been removed, the margins of resection are

    microscopically negative, and no distant metastases were found, is required before

    adjuvant therapy is considered. Resections that leave microscopic or gross residual

    disease are not adjuvant treatment, but rather therapy of known residual cancer.

    The term perioperative chemotherapy (or neoadjuvant chemotherapy) involves the

    use of systemic treatment before definitive, potentially curative surgery.

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    Adjuvant Postoperative Systemic Therapy

    Adjuvant postoperative systemic chemotherapy has not shown a significant

    advantage over surgery alone.

    Postoperative Adjuvant Intraperitoneal Chemotherapy

    Peritoneal recurrence is a common component of the failure pattern for

    patients with gastric cancer. The rationale for the use of intraperitoneal treatment

    is based on the pharmacokinetic observation that drug concentrations within the

    peritoneal cavity after intraperitoneal administration are much higher than those

    achievable intravenously or orally.

    For gastric cancer, an increasing number of reports have been published in

    which immediate postoperative intraperitoneal therapy was given after potentially

    curative resection. However, no definitive conclusions can yet be drawn regarding

    the effectiveness of intraperitoneal postoperative chemotherapy in this setting.

    Immunochemotherapy

    The use of adjuvant immunostimulants (either protein-bound

    polysaccharide (PSK) or a Streptococcus pyrogenes preparation, OK432) given in

    association with cytotoxic chemotherapy has been studied, however larger studies

    that are adequately powered would be necessary to definitively evaluate this

    approach.

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    Perioperative (Neoadjuvant) Chemotherapy

    Perioperative (pre- and postoperative) chemotherapy, also known as

    neoadjuvant chemotherapy, is an attractive concept in gastric cancer because many

    patients, particularly Western patients, have locally advanced tumors at diagnosis

    (T3 or T4, or obvious lymph node involvement).

    Such patients are not only at substantial risk for distant metastasis, but local

    extent of the tumor may make an R0 resection difficult.

    There are two goals to perioperative treatment: reduce the stage of the

    primary tumor to increase the likelihood that a R0 resection can be performed, and

    begin at an early time to treat micrometastatic disease.

    Adjuvant Radiation and Chemoradiation Therapy

    Most of the studies that have evaluated radiation therapy as an adjuvant

    have used concomitant 5-FU chemotherapy. There was a significant improvement

    in survival with the combination of 5-FU and radiation compared with radiation

    alone.

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    Technical Treatment-Related Issues

    Surgery

    Beginning with laparoscopy allows for careful intraoperative staging of

    disease. Inspection for the presence of ascites, hepatic metastases, peritoneal

    seeding, disease in the pelvis (such as a metastasis), or ovarian involvement should

    be performed. Once distant metastases have been ruled out, depending on the

    location of the lesion, a bilateral subcostal incision or a midline abdominal

    incision can be used to gain adequate exposure to the upper abdomen.

    The stomach should be inspected to assess the location and extent of

    tumor. The size and location of the primary tumor dictate the extent of gastric

    resection. A D2 lymphadenectomy sparing the spleen and pancreas can be done

    safely and provides an excellent specimen for surgical and pathologic staging, but

    this procedure should only be performed by or with an experienced surgeon.

    The D2 subtotal gastrectomy commences with mobilization of the greater

    omentum from the transverse colon. After the omentum is mobilized, the anterior

    peritoneal leaf of the transverse mesocolon is incised along the lower border of the

    colon, and a plane is developed down to the head of the pancreas. The infrapyloric

    lymph nodes are dissected and the origin of the right gastroepiploic artery and vein

    are ligated.

    With a combination of blunt and sharp dissection, the plane of dissection

    continues on to the anterior surface of the pancreas, extending to the level of the

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    common hepatic and splenic arteries. This maneuver can be tedious, but

    theoretically it provides additional protection against serosal spread of tumor to

    the local peritoneal surface.

    The right gastric artery is ligated. At this point, the duodenum is divided

    distal to the pylorus. The stomach and omentum are then reflected cephalad. The

    gastro hepatic ligament is divided close to the liver up to the gastro esophageal

    junction. Dissection is then continued on the hepatic artery toward the celiac axis.

    Once near the celiac axis, the lymph node bearing tissue is dissected until

    the left gastric artery is visualized and can be divided at its origin.

    The proximal peritoneal attachments of the stomach and distal esophagus

    can then be incised, and the proximal extent of resection is chosen. For tumors of

    the mid- and proximal stomach, dissection of the lymph nodes along the splenic

    artery and splenic hilum is important.

    This technique is not indicated for antral tumors, given the low rate of

    splenic hilar nodal metastases seen with these tumors. The stomach is then divided

    5 cm proximal to the tumor, which dictates the extent of gastric resection.

    Despite the fact that the entire blood supply of the stomach has been

    interrupted, a cuff of proximal stomach invariably shows good vascularization

    from the feeding distal esophageal arcade.

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    When feasible, most surgeons prefer to anastomose jejunum to stomach

    versus esophagus because of the technical ease and excellent healing.

    Reconstruction using a variety of techniques has been described and is a matter of

    personal choice.

    TREATMENT OF ADVANCED DISEASE (STAGE IV)

    Chemotherapy versus Best Supportive Care

    Patients receiving chemotherapy as part of their treatment have a better

    overall survival than those receiving best supportive care only, with an overall

    hazard ratio of 0.39 (95% CI, 0.28 to 0.52). The median survival was improved

    from 4.3 months for best supportive care to approximately 11 months for

    chemotherapy.

    Single-Agent Chemotherapy

    For most drugs, a variety of doses and schedules have been studied. In the

    absence of comparative trials using the same agent with different doses and

    schedules, superiority of one regimen over the other cannot be assessed.

    Combination Chemotherapy

    Like other malignancies, multidrug regimens using agents that have a

    single-agent activity have been extensively studied in gastric cancer.

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    One of the most widely used combination chemotherapy regimens in upper

    gastrointestinal tract malignancies, including gastric cancer, is the two-drug

    combination of cisplatin and fluorouracil.

    Other combination chemotherapy regimens include methotrexate,

    fluorouracil, and doxorubicin (FAMTX); etoposide, leucovorin, and fluorouracil

    combination; fluorouracil plus irinotecan; docetaxel added cisplatin fluorouracil;

    epirubicin-cisplatin-fluorouracil; irinotecan-fluorouracil-leucovorin ; Cisplatin

    Plus Irinotecan; Fluorouracil-Leucovorin-Oxaliplatin (FOLFOX)

    Targeted Therapy

    Bevacizumab

    As with other solid tumors, including colorectal cancer, breast and lung

    cancers, therapeutic agents with a specific tumor target are now entering study in

    gastric and gastroesophageal junction tumors. One of the first compounds studied

    was bevacizumab, a humanized monoclonal antibody that binds the vascular

    endothelial growth factor ligand. Bevacizumab can safely be given with cytotoxic

    chemotherapy, including in patients in whom the primary tumor was still in place.

    Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors

    Both erlotinib and gefitinib have been studied in gastroesophageal junction

    and gastric cancers. The bulk of the data is currently available only an abstract

    form. Cetuximab, an antibody to the epidermal growth factor receptor, is

    undergoing study as a single agent and also in combination with systemic

    cytotoxic chemotherapy.

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    Radiation for Palliation

    To date, no studies have evaluated the use of radiation therapy in patients

    with locally recurrent or metastatic carcinoma of the stomach. Its use is likely to

    be limited to palliation of symptoms such as bleeding or controlling pain

    secondary to local tumor infiltration.

    Although minimal data are available, radiation therapy seems to be fairly

    effective (from anecdotal experience) in controlling bleeding, as is true in other

    sites. This can often be accomplished at relatively low radiation doses. Pain from

    local tumor invasion can also be palliated, although the dose required is higher (45

    Gy).

    Long-Term Side Effects of Therapy

    Relatively little has been written in the oncology literature on the local

    effects of therapy for gastric cancer and its long-term implications. The presence

    of dumping syndrome is well known, with its resulting diarrhea and cramping, but

    vasomotor effects such as palpitations and diarrhea also occur either very shortly

    after a meal or 1 to 3 hours later. These symptoms probably result from rapid

    transit of food from the stomach into the small bowel with the release of various

    gastrointestinal hormones. These symptoms can be managed by adjusting the

    volume of oral intake and other dietary manipulations. There is also a reactive

    hypoglycemia that can result from the rapid insulin release after a meal with little

    gastric reservoir.In addition to dumping, there are a number of malabsorption

    issues that can be important. B12malabsorption is well known, and many patients

    are placed on monthly supplements, even if it is not clearly needed.

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    After partial gastrectomy one can often monitor B12 levels and replace

    when needed. Iron and calcium absorption is improved by the gastric acid that is

    eliminated or decreased by surgery or radiation therapy, and bypassing the

    duodenum also decreases absorption. Low iron is discovered when patients

    develop an iron deficient anemia, but calcium malabsorption may not be found for

    many years when the patient develops osteopenia. Patients should be followed

    with dual energy x-ray absorptiometry scans and/or placed on calcium

    supplementation (calcium citrate is better absorbed than calcium carbonate).

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    METHODOLOGY

    The present study was undertaken at K.R. Hospital , Mysore from the period

    January 2009 to July 2010 and included patients presenting to the out and in

    patient departments at K.R.Hospital, Mysore. The tissue for diagnosis was

    obtained by endoscopy or following surgical resection.

    Source of Data

    Patients presenting to K.R. Hospital, Mysore during the study period and those

    found eligible were included in the study.

    Sample size: Minimum of twenty five cases meeting criteria of the present study

    Inclusion Criteria

    Only patients with histological proven carcinoma stomach were included

    Exclusion criteria

    Patients with tumour recurrence

    Investigations

    Routine Blood investigations like Haemoglobin%, Total Count, Differential

    Count, Bleeding Time, Clotting time.

    Renal parameters like Blood Urea and Serum Creatinine

    Liver Function Tests

    Serum Electrolytes

    Chest X-Ray

    Blood Grouping

    Special investigationslike Upper Gastointestinal Endoscopy, USG Abdomen and

    CT Scan Abdomen

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    The cases were studied with importance given to clinical history regarding nature

    of presentation including diet history. The study of association of risk factors was

    also undertaken. Thorough clinical examination, Ultrasonography, endoscopy, CT

    in few cases and histopathologic diagnosis formed the basis of the study.

    The anatomic site of occurrence, the macroscopic type and the histopathologic

    type were studied in each case.

    An earnest attempt was made to study all the cases in detail with serial follow-up,

    the latter being incomplete due to non-responsive patients.

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    RESULTS

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    RESULTS

    ANNUAL PREVALENCE: Graph-1

    Gastric carcinoma is a common cancer with almost evenly distributed

    annual prevalence.

    The number of cases reported was greater in the first half of the year.

    Graph-1

    Annual distribution of cases from 2009 to July 2010

    0

    2

    46

    8

    Jan Feb Mar Apr May Jun Jul Aug Sep Oct Nov Dec

    No.ofcas

    es

    2010

    2009

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    SEX PREVALENCE: Table 7; Graph 2

    Gastric cancer is more common in males with 75% of the cases being

    males in this study. The Male: Female ratio was 3:1.

    Table-7. Sex distribution among carcinoma stomach patients

    SexPresent study

    Cases %

    Male 24 75

    Female 8 25

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    AGE PREVALENCE: Table 8; Graph 3

    Carcinoma stomach is more common in the older age group with

    increasing incidence after the age forty five. The maximum number of cases was

    seen between the age groups 45 to 65. The youngest patient was aged 33 and the

    oldest 79.

    Table-8. Age distribution among carcinoma stomach patients

    AgePresent study

    Total % M F

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    SOCIOECONOMIC STATUS: Table 9; Graph 4

    In the present study majority of the patients(75%) belonged to the low

    socioeconomic status. The prevalence among the high socioeconomic group could

    not be studied as none of the patients belonged to this strata.

    Table 9- Income group among carcinoma stomach patients

    Income Group Present study

    Cases %

    Low 28 87.5

    Middle 4 12.5

    High 0 -

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    RISK FACTORS: Table 10; Graph 5.0, 5.1

    There are strong suggestions of the influence of environmental factors on

    gastric cancer. The most common risk factors associated were spicy food and

    mixed diet followed by tobacco and alcohol use.

    In this study twenty seven(84.4%) patients consumed mixed diet and the

    rest were vegetarians. The non vegetarians took meat/fish approx. thrice every

    week.

    All patients in the study group frequently and regularly consumed green

    leafy vegetables.

    Fruit consumption was frequent only in twenty two(68.7%) of the cases

    with predominant of them being males(86.4%). Only three(13.6%) of the females

    frequently consumed fruits.

    High salt intake was not reported by any of the subjects in this study

    although this value was not quantified and hence significance could not be

    ascertained.

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    Smoked foods though a common risk factor in many countries was

    consumed only by Five (15.6%) of the patients and even in theses patients the

    intake was not frequent. Majority of the patients, twenty seven(84.4%) reported to

    the use of high spicy diet in everyday food.

    Tobacco smoking in the form of cigarette and beedi smoking was seen in

    nineteen (59.3%) patients, all being males. Five females and three males reported

    to frequent use of betelnut which has been shown to a risk factor in the

    development of gastric cancer.

    Alcohol consumption was seen in sixteen(50%) of the patients, all males,

    who consumed it regularly and for a period of more than ten years.

    Table 10 - Comparision of risk factors between males and females, F- Frequent,O-Occasional

    Risk factor Total Males(24) Females(8)

    Cases % Cases % Cases %

    Mixed diet 27 84.4 20 74.1 7 25.9

    Veg diet 5 15.6 4 80 1 20

    Green leafy F 32 100 24 75 8 25

    O 0 0 - 0 -

    Fruits F 22 68.7 19 86.4 3 13.6

    O 10 31.3 5 50 5 50

    High salt intake 0 - - - -

    Smoked Foods 5 15.6 4 80 1 20

    Spicy 27 84.4 21 77.7 6 22.2

    Smoking 19 59.3 19 100 - -

    Alcohol 16 50 16 100 - -

    Betel nut 8 25 3 37.5 5 62.5

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    BLOOD GROUP: Table 11; Graph 6

    Blood group A showed the highest association with gastric cancer patients

    with fourteen(43.7%) cases followed by blood group O and B.

    Table 11 - Blood group distribution in carcinoma stomach patients

    Study Blood Group (%)A + B+ AB+ O+

    Present Study 14(43.7) 5(15.6) 1(3.1) 12(37.5)

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    SYMPTOMS: Table 12, Graph 7

    Anorexia was the most common symptom in patients and was reported in

    twenty six (81.25%) of the patients. The next most common symptom was nausea

    and vomiting reflecting the high prevalence of distal tumours. Twenty three

    (71.8%) reported weight >10% of body weight.

    Proximal tumours involving the gastooesophageal junction had dysphagia

    as the predominant symptom. Only one patient in this study presented with

    jaundice and none of the patients had supraclavicular lymphadenopathy at

    presentation. One patient presented with features of peritonitis and was found to

    have a growth in the body of the stomach which had perforated.

    Early satiety was reported in sixteen (50%) of the patients which is

    characteristic of tumours involving the stomach wall diffusely.

    Symptom analysis among the two sexes revealed that nausea, vomiting and

    weight loss were the most common symptoms followed by pain abdomen in

    females. The most common symptoms in males were anorexia, abdominal pain

    followed by nausea and vomiting.

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    Table 12-Symptom analysis in patients of carcinoma stomach

    Symptoms

    Present study Males n=24 Females n=8

    Cases % Cases % Cases %

    Abdominal Pain 22 68.75 16 66.6 6 75

    Nausea/vomiting 24 75 19 79.2 5 62.5

    Weight loss 23 71.8 15 62.5 8 100

    Anorexia 26 81.25 18 75 8 100

    Early satiety 16 50 12 50 4 50

    Jaundice 1 3.2 1 4.2 - -

    Dysphagia 5 15.6 4 16.6 1 12.5

    Malaena 7 21.8 5 20.8 2 24

    Others 2 6.25 1 4.4 1 12.5

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    SIGNS: Table 13, Graph 8

    Overall, anemia was the most common sign in twenty one (65.6%) of the

    cases followed by dehydration and ascites.

    Visible gastric peristalsis the characteristic sign of gastric cancer was seen

    only in four (12.5%) of the cases. Gastric cancer presented as mass abdomen in

    six (18.75%) cases.

    In females, anemia and ascites were the most common symptoms. None of

    the females in this study had visible gastric peristalsis which was seen in three

    (12.5%) of males.

    Presentation with mass abdomen was commoner in females (37.5%) than

    in males (12.5%).

    Ascites at presentation suggesting the advanced stage of the disease was

    more common in females (50%) compared to males (31.25%).

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    Table 13 - Analysis of signs in gastric cancer patients

    Signs Total

    cases

    % Male n=24 Female n=8

    Cases % Cases %

    Anemia 21 65.6 14 58.3 7 87.5

    Icterus 1 3.12 1 4.2 - -

    Dehydration 10 31.25 7 29.2 3 37.5

    Ascites 10 31.25 6 25 4 50

    VGP 4 12.5 4 16.6 - -

    Mass abdomen 6 18.75 3 12.5 3 37.5

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    SUBSITES: Table 14; Graph 9

    The antrum was the most common site of affliction accounting for 75% of

    all subsites. This was also similar in both the sexes with percentages of 70.8 in

    males and 87.5 in females. Oesophagogastric tumours accounted for 9.37% of the

    cases and were similar in both the sexes. None of the females in this study had

    cancers of the body and proximal stomach.

    Table 14- Sub site specific trends in carcinoma stomach

    Sub site Total Male Female

    Cases % Cases % Cases %

    Oesophagogastric jn 3 9.37 2 8.3 1 12.5

    Proximal stomach 2 6.25 2 8. 0 -

    Body 3 9.37 3 12.5 0 -

    Antrum 24 75 17 70.83 7 87.5

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    MACROSCOPY: Table 15

    The


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