Journal
ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
Volume 10, Issue 2, Pages 111-115Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/187152010790909326
Keywords
BCR-ABL; leukemic stem cells; CML; therapeutic agents
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Funding
- NCI NIH HHS [R01 CA122142-04, R01 CA114199-05, R01 CA122142, R01 CA122142-03, R01 CA114199-04, R01 CA122142-05, R01 CA114199] Funding Source: Medline
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Chronic myeloid leukemia (CML) is induced by the BCR-ABL oncogene, a product of Philadelphia (Ph) chromosome. The BCR-ABL kinase inhibitor imatinib is a standard treatment for Ph+ leukemia, and has been shown to induce a complete hematologic and cytogenetic response in most chronic phrase CML patients. However, imatinib does not cure CML, and one of the reasons is that imatinib does not kill leukemia stem cells (LSCs) in CML both in vitro and in vivo. Recently, several new targets or drugs have been reported to inhibit LSCs in cultured human CD34(+) CML cells or in mouse model of BCR-ABL induced CML, including an Alox5 pathway inhibitor, Hsp90 inhibitors, omacetaxine, hedgehog inhibitor and BMS-214662. Specific targeting of LSCs but not normal stem cell is a correct strategy for developing new anti-cancer therapies in the future.
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