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LEUKEMIA
Dr. SUHAEMI, SpPD, FINASIM
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8 Parameter Cell Counter
WBC: White BloodCells
RBC: Red Blood Cells HgB: Hemoglobin
Hct: Hematocrit
MCV: Mean Cell
Volume
MCH: Mean CellHemoglobin
MCHC: Mean CellHemoglobinConcentration
RDWt: Red Blood Cell
Distribution Width
Biomedica Diagnostics Inc. / D. Jette / March 2003 2
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Normal Values
Hematocrit = 40 to 54 %
Hemoglobin = 13.5 to 18 g/dL
Red Cells = 4.6 to 6.3 x 106 cells / L
White Cells = 4.5 to 11 x 103 cells / L
Platelets = 150 to 450 x 103 cells / L
Biomedica Diagnostics Inc. / D. Jette / March 2003 3
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PENDAHULUAN
Leukemia merupakan penyakit keganasan seldarah yang berasal dari sumsum tulang ditandaioleh proliferasi sel sel darah putih, denganmanifestasi adanya sel sel abnormal dalamdarah tepi.
Leukosit dalam darah berpoliferasi secara tidakteratur dan tidak terkendali dan fungsinyapunmenjadi tidak normal
Oleh karena proses tsb fungsi-fungsi lain dari seldarah normal juga terganggu hinggamenimbulkan gejala leukemia yang dikenaldalam klinik
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What Is Leukemia?
Cancer of the white blood cells
Acute or Chronic
Affects ability to produce normal blood cells
Bone marrow makes abnormally largenumber of immature white blood cells called
blasts
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Leukemia
Hallmark: proliferation of malignant cells inthe bone marrow
Divided into: acute v. chronic
lymphoblastic v. myeloid (non-lymphoblastic)
Each type of leukemia has a differentpresentation, natural history, prognosis, andtreatment.
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Classification of leukaemias
Acute Chronic
Myeloidorigin
Lymphoidorigin
Acute MyeloidLeukaemia (AML)
Acute LymphoblasticLeukaemia (ALL)
Chronic Myeloid Leukaemia (CML)
Chronic Lymphocytic Leukaemia(CLL)
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Leukemia
Acute leukemias: rapid onset, rapid death iftreatment is not successful
Chronic leukemias: natural history measuredin years, even without initial treatment
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FAB (1976) Classification
M0 -- Undifferentiated AML
M1 -- AML without maturation
M2 -- AML with maturation M3 -- Acute Promyelocytic Leukemia
M4 -- Acute Meylomonocytic Leukemia
M5 -- Acute Monocytic Leukemia
M6 -- Erythroleukemia (DiGuglielmos)
M7 -- Megakaryoblastic Leukemia
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M1 and M2
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M3
M5
M4
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Acute Leukemia
Presenting features: Anemia
Fatigue, dyspnea, angina pectoris
Neutropenia - the leukocyte count may be high or
low, but neutropenia is characteristic Unexplained fever, serious infections
Thrombocytopenia
Bruising, petechiae
Less common: lymphadenopathy, splenomegaly, skininfiltration, chloromas (tumors composed ofmalignant marrow cells)
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Acute Leukemia
Diagnosis: >20% blasts in the bone marrow
Categorized by
H&E staining Cytochemical stains (myeloperoxidase, NSE)
Flow cytometry
Cytogenetics
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Acute Leukemia
No evidence of maturation withinblood or marrow
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What is AML?
The term Myelogenous
denotes what type of
cell is being affected:
Monocytes andNeutrophils
Acute refers to rapid
progression formingimmature cells
Results from acquired
genetic damage to the
DNA of the bone
marrow
Immature cells
produced are known as
blast cells
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SIMPLIFIED SCHEMA OF
HEMATOPOETIC CANCERS
Hematopoetic
Stem Cell
Myeloid
Lymphoid
Acute and chronic
Myeloid Leukemias
Lymphomas
Hodgkins (30%)
Non Hodgkins (70%)
WBC
RBC
Platelets
B Cells
T cells
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Haematopoiesis
PLURIPOTENT
STEM CELL
COMMITTED
PROGENITOR
CELL
RECOGNIZABLE
BONE MARROW
PRECURSOR CELL
MATURE
BLOOD
CELL
myeloblast
monoblast
pronormoblast red cell
neutrophil
monocyte
basophil
platelet
CFU-Baso
CFU-Eos
CFU-GM
BFU-E/CFU-E
eosinophil
pre-T
pre-B
myeloid
progenitor
cell
lymphoid
progenitorcell
lymphoblast
lymphoblast
T-cell
B-cell& plasma cell
MIXED
PROGENITOR
CELL
CFU-Meg megakaryocyte
pluripotent
stem cell
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Hematopoieticstem cell
Neutrophils
Eosinophils
Basophils
Monocytes
Platelets
Red cells
Myeloidprogenitor
Lymphoidprogenitor
B-lymphocytes
T-lymphocytes
Plasmacells
nave
ALL
AML
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Where AML Originates
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Genetic Associations
Research states that AML is caused by geneticaberrations such as translocations betweenchromosomes that alter the function oftranscriptory regulatory factors
These translocations are a direct result ofchimeric fusion proteins which are caused by theabnormal cells and its inability to allow furthergrowth, proliferation, maturation and
differentiation. Class 1 and 2: mutations responsible for the
development of the neoplastic process ofmyeloproliferation and de-differentiation
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Genetic Associations
Continued Class 1: mutations that give rise to proliferation
and/or differentiation and are made from
tyrosine kinases (TK); they have no affect on
differentiation
Class 2: mutations that interfere with terminal
differentiation and apoptosis thereby providing
survival advantage for the mutated cells;associated with Core Binding Factors (CBFs)
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differentiationblock
enhancedproliferation
AcuteLeukemia
+
Gain of function mutations oftyrosine kinases
eg. FLT3, c-KIT mutations
N- and K-RAS mutationsBCR-ABL
TEL-PDGFbR
Loss of function oftranscription factorsneeded for differentiation
eg. AML1-ETOCBFb-SMMHCPML-RARa
Two-hit model of
leukemogenesis
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Tyrosine Kinases
Tyrosine kinases are alsoknown as oncogenes
Oncogenes are present inthe mutated neutrophilsand moncytes
AML activates themcausing uncontrollable
proliferation, apoptosis,decreased adhesion, andinhibits differentiation
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Causes of acute leukemias
idiopathic (most)
underlying hematologic disorders
chemicals, drugs ionizing radiation
viruses (HTLV I)
hereditary/genetic conditions
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AML and its Impact on the
Immune System AML affects the innate immune system
Secondary Immune System kicks in
The proliferation of immature neutrophilsand moncytes takes place
Unable to leave the bone marrow to go intoblood stream and tissues to fight offinfections
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Main Types
Acute Lymphocytic Leukemia (ALL)
Acute Mylogenous Leukemia (AML)
Chronic Lymphocytic Leukemia (CLL)
Chronic Mylogenous Leukemia (CML)
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Symptoms
When there are excessive white blood cells --> Infections
When there are few red blood cells: Paleness--> Anemia
When there are few platelets --> Excessive
bleeding
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Tests For Diagnosis
Finger prick
Blood sample
Blood dye
Bone marrow sample
Spinal Tap/Lumbar Puncture
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Flow cytometry:
CD3 (T-lineage ALL)
CD19 (B-lineage ALL)
Cytogenetics:
t(22;9)
t(4;11)
t(2;8)
t(8;14))
Lab Studies
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Coagulogramm:
elevated prothrombin time
decreased fibrinogen levels
presence of fibrin split products
Chemistry profile:
elevated lactic dehydrogenase level
elevated uric acid levelliver function tests
BUN/creatinine determinations
Lab Studies
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Cytogenetics
Technique Needs dividing cells, so marrow usually better
Complemented and extended by FISH and
rtPCR FISH: Fluorescence In Situ Hybridization
Typically in metaphase cells, peripheral blood worksfine- so ideal when marrow unavailable
rtPCR- for 15;17
rtPCR for BCR:ABL in ALL
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Cytogenetics
Good (thats a laugh) 15;17
8;21
M2, AML with differentiation, often with CD19 Core binding factor
INV16 M4eo, basophilic eosinophils in marrow
Watch for CNS disease
Core binding factor
These abnormalities typically trump bad riskcytogenetics.
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Cytogenetics
Intermediate
Normal
One or two abnormalities
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Cytogenetics
Bad
Chromosome 7
Chromosome 5
Complex (3 or more)
11q23
Any trisomy?
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Management:
A-Supportive measure:-isolation in positive laminer flux room
-insertion of central line
-family and patient support by permanent social worker
-AlKaline diuresis to prevent tumor lysis syndrome
-oropharynx/GIT decontamination to prevent fungalinfection
-IV antibiotics for infection
-Blood transfusion if anemia and thrombocytopenia.
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Therapeutic option
B-Curative intent:only allogenic bone marrow transplant .
C_Classical approch(curative/palliative)-induction chemotherapy
-consolidation of remission
-intensification
-maintenance chemotherapy
-CNS prophylaxis
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Medical Care
Induction therapy:
4-drug regimen of vincristine, prednisone,anthracycline, and cyclophosphamide or L-asparaginase or a 5-drug regimen of vincristine,prednisone, anthracycline, cyclophosphamide, and L-asparaginase given over the course of 4-6 weeks.
Consolidation therapy:
a standard 4- to 5-drug induction usually include
consolidation therapy with Ara-C in combination withan anthracycline or epipodophyllotoxin.
Maintenance
CNS prophylaxis
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AML therapy
Cytarabine Infusional or high-dose
Anthracycline Any will do- dauno, ida, mitoxantrone
Other active agents Etoposide
Cyclophosphamide
Hydroxyurea
6MP/TG
Topotecan
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Replacement of blood products: packed red bloodcells, platelets, fresh frozen plasma
Antibiotics: a third-generation cephalosporin (orequivalent) with an aminoglycoside. Patients with
persistent fever after 3-5 days of antibacterialantibiotics have amphotericin added to their regimen.
The use of prophylactic antibiotics in neutropenicpatients who are not febrile is controversial. Acommonly used regimen includes ciprofloxacin (500
mg orally twice daily, fluconazole (Diflucan) (200 mgorally daily), and acyclovir (200 mg orally 5 times/d).
Supportive Care
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Growth factors
Allopurinol 300 mg 1-3 times/d
Central venous catheter
Supportive Care
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Prognosis
Good risk includes (1) no adverse cytogenetics, (2) ageyounger than 30 years, (3) WBC count of less than30,000/mL, and (4) complete remission within 4weeks.
Intermediate risk does not meet the criteria for eithergood risk or poor risk.
Poor risk includes (1) adverse cytogenetics [(t9;22),(4;11)], (2) age older than 60 years, (3) precursor B-cell
WBCs with WBC count greater than 100,000/mL, or (4)failure to achieve complete remission within 4 weeks.
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Prognosis
Genetic abnormalities:
t(9;22) - poor outlook
t(4;11) - younger age, female predominance,
high white cell counts, and L1 morphologyt(8;14) - older age, male predominance, frequent
CNS involvement, and L3 morphology
Both are associated with a poor prognosis.
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Prognosis in AML
parameters Favorable unfavorable
Cytogentics T(15;17).
T(8;21).Inv(16).
Deletion of chromosome5or7.
11q23T(6;9)
Abn(3q)complex
rearrangments
BM response toremission induction
20% blasts after first course.
age 60yrs
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Differential diagnosis of Acuteleukemias:
Lymphoma.
Myelodysplastic syndrome.
Multiple myeloma. Aplastic anemia
Sever megaloblastic anemia due to B12
defeciency. Severe lymphocytosis due to infections.
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Myeloid maturation
myeloblast promyelocyte myelocyte metamyelocyte band neutrophil
MATURATION
Adapted and modified from U Va website
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Erythrocytes
Normal range 4.2-5.5 million per
mm3 in adults.
Biconcave shape.
Diameter 7
microns.
Cells for transport
of O2 and CO2.
Life span 120
days.
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Leukocytes
Normal range 4 -
11 thousand per
mm3 in adults.
Five types.
Size 8-20 microns. Involved in
fighting infection,
combatting
allergic reactions,
and immune
responses.
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Thrombocytes
Smallest cells in
the blood.
Normal range
130,000-400,000. Active role in
coagulation and
hemostasis.
i f
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Pictures Of Blood
Normal human blood
White Cell Red Cell
Platelet
Blood with leukemia
BlastsRed Cell
Platelet
White Cell
Sources fromArginine.umdnj.eduSources from beyond2000.com
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Acute Myelogenous Leukemia:
Auer Rod
Blasts
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Blasts
Acute Myelogenous Leukemia with differentiation
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Petechiae
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Infiltration of
tissues/organs enlargement of liver, spleen, lymph nodes
gum hypertrophy
bone pain other organs: CNS, skin, testis, any organ
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Gum hypertrophy
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AML gingival hypertrophy
Gi i l I filt ti i
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Gingival Infiltration in
Monocytic (AML M4 eos) Variant of
AML
Mani, A, Lee, DA. Leukemic Gingival Infiltration. N Engl J Med 2008; 358(3): 274. Copyright 2008 Massachusetts Medical Society
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A
B
C
Chloromas
NEJM 1998
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Effects On the Body
Attacks the immune system
Infections
Anemia Weakness
No more regular white blood cells, red blood cells,
and platelets Blasts clog blood stream and bone marrow
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Causes
High level radiation/toxin exposure
Viruses
Genes
Chemicals
Mostly unknown Cant be caught
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Treatment
Chemotherapy
Immunotherapy
Radiation
Bone marrow transplant
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Research
New drugs
Cord blood and planceta
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Myeloblasts with auer rods
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Lymphoblast
AML
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Auer rods in AML
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LEUKEMIA LIMFOBLASTIK AKUT
LLA merupakan leukemia yg paling seringdijumpai pada anak anak.
Pada anak kecil ditandai dgn mendadakpanas,pucat dan memar di kulit.
Sering dijumpai nyeri di tulang beberapa bulansebelum timbul ekimosis,pucat dan panasbadan.
Perasaan lemah, BB tidak bertambah/menurun,
nafsu makan menurun, kadang kadangepistaksis atau perdarahan gusi dapatmerupakan keluhan tambahan.
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PEMERIKSAAN FISIK
Anak terlihat pucat, tampak sakit berat,takikardi dan bisa dijumpai perdarahanfundus oculi.
Limfadenopati di leher,aksila dan inguinal,bisa bersifat simetris.
Hepatosplenomegali.
Stadium awal CNS tidak terlibat Stadium lanjut terlihat gejala rangsangan
meningens dan gejala serebral dgn timbulnyarefleks patologis
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TERAPI
Kemoterapi
Radiasi CNS
ALL
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ALL-L1
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ALL-L2
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LEUKEMIA LIMFOSITIK KRONIK
LLK adalah jenis leukemia yg paling seringpada orang tua, biasanya asimtomatik.
Biasanya ditemukan pada saat pemeriksaandarah rutin atau pada seseorang dgnhepatosplenomegali atau limfadenopati ygasimptomatik.
Keadaan asimptomatik dapat berlangsungbertahun tahun sampai timbul keluhanleukemianya
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Chronic Lymphocytic leukemia
Commonest leukemia in the western world
Clonal proliferation of the B-Lymphocytes
Disease of the elderly
Younger patients now seen
M:F ratio, 2:1
CLL is highly variable disorder
75% cases, diagnosis by chance on a routineblood test
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Chronic Lymphocytic Leukemia
Age: the elderly
Prognosis: may live for many years evenwithout treatment
Treatment: Watchful waiting, purinenucleoside analogues (fludarabine), alkylators
Lymphocytosis
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Lymphocytosis
Chronic Lymphocytic Leukemia
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Chronic Lymphocytic Leukemia
Clonal proliferation of lymphocytes
-95 % with B-cell phenotype
Usually detected as an asymptomaticlymphocytosis
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CLLPB and BM
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Chronic Lymphocytic Leukemia
Hypogammaglobulinemia is common
Infection is the most common cause of death
Complications can include AIHA & ITP May transform into an aggressive lymphoma
Two staging systems exist: Rai & BinetEarly stage disease has a survival equivalent to age-
and sex-matched controls
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Most patients do not require specific treatment
Indications for treatment
anemia
thrombocytopenia
unsightly adenopathy
other complications
When treatment is needed, alkylators or
pur ine nucleoside analoguesare used
Aetiology
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Aetiology
Cause unknown
Not associated with radiation or exposure tooccupational hazards
Among the leukemias, CLL has the strongesttendency for familial incidence
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h i l k i
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Chronic Myelogenous Leukemia
CML adalah leukemia yang sering mengenaiorang dewasa, kadang kadang pada anak danusila.
Gejala yg diketemukan adalah penurunanberat badan, nafsumakan berkurang,perasaan cepat letih, cepat kenyang ok
splenomegali
h i l k i
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Chronic Myelogenous Leukemia
Age: adults
Prognosis: 3-4 years without BMT, curespossible with BMT
Treatment:
Imatinib (Gleevec)
Bone marrow transplant
Hydroxyurea +/- interferon;
h i l k i
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Chronic Myelogenous Leukemia
Leukocytosis with all degrees of myeloiddifferentiation in blood and marrow
Often associated with eosinophilia,
basophilia, thrombocytosis
Splenomegaly is characteristic
Ch i M l L k i
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Chronic Myelogenous Leukemia:
Philadelphia Chromosome
9;22 translocation yields a chimeric genetermed bcr-abl
bcr derived from chromosome 22
abl derived from c-abl oncogene on chrom. 9
Encodes a 210,000 MW protein - a tyrosineprotein kinase
Ability to detect transcript by PCR mayenable us to detect molecular remissions
Ch i M l L k i
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Chronic Myelogenous Leukemia
Disease terminates in blast crisis in 3-4 years; thisresponds to treatment poorly, and is rapidly fatal
Blast crisis may have the phenotype of non-myeloid cells
Leukocyte count > 200 x 109/L may be associated
with leukostasis
Allogeneic BMT has been the treatment of choice ifthe patient is a candidate
Imatinib is a new option
Ch i M l L k i
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Chronic Myelogenous Leukemia:
Results of BMT
Five year survival > 60% with allogeneic BMT
< 25% of patients have an HLA-matchedsibling
Matched unrelated donors (MUD) may beused
Ch i M l L k i
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Chronic Myelogenous Leukemia
Other approaches
Imatinib (Gleevec): Abl tyrosine kinase inhibitor:dramatic responses
A classic example of targeted therapy
Probably not a cure, but a remarkable advance 87% major genetic response in chronic phase
55% response in blast crisis
Alpha-interferon 34.7 % major genetic response
Hydroxyurea or alkylators can control leukocytosis
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Chronic Myelogenous Leukemia
PMN
Band
Eosinophil
Basophil
Early Myeloid
Cells
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BCR ABL translocation
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BCR-ABL translocation
Chronic Myelogenous Leukemia
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FISH showing the BCR (green), ABL (orange), and BCR-ABL fusion signals (arrow):A=positive (contains a residual ABL signal), B=normal
Jemshidi trephine &
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p
Salah aspiration needle
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Chemotherapy - Uses drugs to kill leukemia cells.
Radiation therapy - uses high-energy rays to killleukemia cells.
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Stem cell transplant - treated with high doses of drugs,
radiation, or both which destroy both leukemia cells and normal
blood cells in the bone marrow. Later, the patient receives
healthy stem cells and new blood cells develop from the
transplanted stem cells. (Ex. Bone Marrow Transplant)