期刊
LEUKEMIA
卷 24, 期 9, 页码 1545-1554出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2010.143
关键词
BCR-ABL; leukemic stem cells; CML; therapeutic agents
资金
- NCI NIH HHS [R01 CA122142-05, R01 CA122142-03, R01 CA114199, R01 CA122142-04, R01 CA114199-05, R01 CA122142] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA122142, R01CA114199] Funding Source: NIH RePORTER
Inhibition of BCR-ABL with kinase inhibitors in the treatment of Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) is highly effective in controlling but not curing the disease. This is largely due to the inability of these kinase inhibitors to kill leukemia stem cells (LSCs) responsible for disease relapse. This stem cell resistance is not associated with the BCR-ABL kinase domain mutations resistant to kinase inhibitors. Development of curative therapies for CML requires the identification of crucial molecular pathways responsible for the survival and self-renewal of LSCs. In this review, we will discuss our current understanding of these crucial molecular pathways in LSCs and the available therapeutic strategies for targeting these stem cells in CML. Leukemia (2010) 24, 1545-1554; doi:10.1038/leu.2010.143; published online 24 June 2010
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