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2010 ; 1
(2
): 124-32
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Molecular and cellular bases of chronic myeloid leukemia
#MMPMID21203982
Chen Y
; Peng C
; Li D
; Li S
Protein Cell
2010[Feb]; 1
(2
): 124-32
PMID21203982
show ga
Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by
the overproduction of granulocytes, which leads to high white blood cell counts
and splenomegaly in patients. Based on clinical symptoms and laboratory findings,
CML is classified into three clinical phases, often starting with a chronic
phase, progressing to an accelerated phase and ultimately ending in a terminal
phase called blast crisis. Blast crisis phase of CML is clinically similar to an
acute leukemia; in particular, B-cell acute lymphoblastic leukemia (B-ALL) is a
severe form of acute leukemia in blast crisis, and there is no effective therapy
for it yet. CML is induced by the BCR-ABL oncogene, whose gene product is a
BCR-ABL tyrosine kinase. Currently, inhibition of BCR-ABL kinase activity by its
kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic
strategy for CML. However, the inability of BCR-ABL kinase inhibitors to
completely kill leukemia stem cells (LSCs) indicates that these kinase inhibitors
are unlikely to cure CML. In addition, drug resistance due to the development of
BCRABL mutations occurs before and during treatment of CML with kinase
inhibitors. A critical issue to resolve this problem is to fully understand the
biology of LSCs, and to identify key genes that play significant roles in
survival and self-renewal of LSCs. In this review, we will focus on LSCs in CML
by summarizing and discussing available experimental results, including the
original studies from our own laboratory.
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