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Chronic Myeloid

Leukemia
Dr. Naveed Akhtar

CHROMIC LEUKEMIA
The chronic leukemias are a group of
malignancies
involving
the
hematopoietic
system
which
progress slowly.There is an increase
of abnormal white blood cells. It
differs fromacute leukemia

TYPE OF CHRONIC LEUKEMIA


Chronic Lymphocytic Leukemia (CLL)

Chronic Myeloid Leukemia(CML)

DEFINITION OF CML
CML is a clonal disorder of a pluripotent stem cell and
is classifi ed as one of the myeloproliferative disorder.

TYPES OF CHRONIC MYELOID


LEUKEMIA
WHO 2008
Myeloproliferative
neoplasms

Old Classification
Chronic Myeloid
leukaemias

Ch.myelogenous leukemia

Polycythemia vera
Essential thrombocythemia
Primary myelofi brosis
Chronic neutrophilic leuke
Chronic eosinophilic leuke
Mast cell disease
MPNs, unclassifi able

CML, Ph positive
CML, Ph- (atypical)
CGL
Juvenile CML
Ch. Neutrophilic
leukaemia
Eosinophilic
leukaemia
Ch. Myelomonocytic
Leuk (CMML)

CHRONIC MYELOGENOUS
LEUKAEMIA
Chronic Myelogenous/Myeloid
Leukaemia (CML) is a
myeloproliferative neoplasm that
originates in an abnormal
pluripotent bone marrow stem cell
and is consistently associated with
the BCR-ABL1 fusion gene located in
the Philadelphia chromosome

CHRONIC MYELOID LEUKEMIA


CML is a myeloproliferative disorder
characterized by increased proliferation of
the granulocytic cell line without the loss of
their capacity to diff erentiate. Consequently,
the peripheral blood cell profi le shows an
increased number of
granulocytes and their
immature precursors,
including occasional
blast cells.

EPIDEMIOLOGY
The disease accounts for around
15% of leukemia.
May occur at any age.

MYELOID DEVELOPMENT STAGES

PHILADELPHIA CHROMOSOME

PHILADELPHIA CHROMOSOME
Is the chromosome which result
from the t(9;22)(q34;q11)part of
the Abelson proto-oncogene ABL is
moved
to
the
BCR
gene
on
chromosome
22
&
part
of
chromosome
22
moves
to
chromosome
9.
The
abnormal
chromosome 22 is the Ph.

CLINICAL PRESENTATION
can occur in any age .But the
mostly between 40-60.
Symptoms related to hyper
metabolism:
weight loss,lassitude,anorexia or night sweats

Gout or renal impairment


caused by hyperuriceamia.
Bone marrow failure: Anemia.

Platelet dysfunction.Bruising,
epistaxis, menorrhagia or
hemorrhage
Organ infiltration:
Splenomegally almost always
present and massive.
Rare symptoms include
visual disturbance.

PHASES OF CML
Chronic phase
Accelerated phase
Blast phase

CHRONIC PHASE

Blasts usually less than 2% TLC


Absolute basophilia invariably present
eosinophilia common
Blast less than 5% of the marrow cells

ACCELERATED PHASE

Blasts more than 10%


but less than 20

BLAST PHASE

Blasts more than 20%

INVESTIGATION:
CBC:
Wbc is usually >50X10/l
& some times >500X10/l.
Normocytic normochromic anemia.
Platelets .
Peripheral blood fi lm:
circulating basophil.
Eosinophil

INVESTIGATIONS
Neutrophil alkaline phosphatase
score is invariably low. But in
infection it is very high

INVESTIGATIONS
BM: hypercellular with granulopoietic
predominance .

INVESTIGATIONS
Cytogenetics/ FISH/ PCR:
Detect pheladelphia
chromosome.

FISH
The dual-color ABL (green) and
BCR (red) probes span their respective
breakpoint regions, producing two red
and two green

INVESTIGATIONS
JAK2 V617F Mutation
S.vitamin B12 & vitamin B12binding capacity are.
S.Uric acid is usually.

TREATMENT
Chemotherapy:
Tyrosine kinase inhibitor:
Interferon-.
Stem cell transplant.

COURSE & PROGNOSIS


Usually shows excellent response to
chemtherapy in the chonic phase.
Death usually occur from terminal
acute trasformation ,hemorrhage or
infection.

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