期刊
GENES & DEVELOPMENT
卷 26, 期 2, 页码 120-125出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.182980.111
关键词
acute myeloid leukemia; apoptosis; Mcl-1; Bcl-x(L)
资金
- Deutsche Forschungsgemeinschaft (DFG)
- Lady Tata Memorial Trust
- NHMRC [257500, 461221, 637326, 1008329, 356203, 461299, 575501, 361646]
- Leukemia and Lymphoma Society (SCOR) [7413]
- NIH [CA43540, CA80188]
- Victorian Cancer Agency
- Leukemia Foundation of Australia
- Australian Cancer Research Fund
- Australian Government (IRISS)
- Victorian State Government (OIS)
Acute myeloid leukemia (AML) frequently relapses after initial treatment. Drug resistance in AML has been attributed to high levels of the anti-apoptotic Bcl-2 family members Bcl-x(L) and Mcl-1. Here we report that removal of Mcl-1, but not loss or pharmacological blockade of Bcl-x(L), Bcl-2, or Bcl-w, caused the death of transformed AML and could cure disease in AML-afflicted mice. Enforced expression of selective inhibitors of prosurvival Bcl-2 family members revealed that Mcl-1 is critical for survival of human AML cells. Thus, targeting of Mcl-1 or regulators of its expression may be a useful strategy for the treatment of AML.
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