Journal
CELL CYCLE
Volume 8, Issue 9, Pages 1338-1343Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.8.9.8209
Keywords
chronic myeloid leukemia; BCR-ABL; p210; GMP; cancer stem cell; leukemia-initiating cell
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Funding
- NCI NIH HHS [R01 CA043054-23, T32 CA067754, R01 CA043054] Funding Source: Medline
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The success of imatinib mesylate (STI571, Gleevec) in treating chronic myeloid leukemia (CML) is, to date, the crowning achievement of targeted molecular therapy in cancer. Nearly 90% of newly diagnosed patients treated with imatinib in the chronic phase of the disease achieve a complete cytogenetic response. However, more than 95% of these patients retain detectable levels of BCR-ABL mRNA and patients discontinuing imatinib therapy almost invariably relapse, demonstrating that an imatinib insensitive population of leukemia-initiating cells (LICs) persists in nearly all patients. These findings underscore the need for treatments specifically targeting the leukemia-initiating population of CML cells. While mounting evidence suggests that the LIC in the chronic phase of CML is the BCR-ABL positive hematopoietic stem cell, several recent publications suggest that during CML blast crisis, a granulocyte-macrophage progenitor (GMP) population also acquires LIC properties through activation of the beta-catenin pathway. Characterization of these cells and evaluation of their sensitivity to imatinib is critical to our understanding and treatment of CML blast crisis.
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