| Literature DB >> 22279045 |
Stefan P Glaser1, Erinna F Lee, Evelyn Trounson, Philippe Bouillet, Andrew Wei, W Douglas Fairlie, David J Izon, Johannes Zuber, Amy R Rappaport, Marco J Herold, Warren S Alexander, Scott W Lowe, Lorraine Robb, Andreas Strasser.
Abstract
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.Entities:
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Year: 2012 PMID: 22279045 PMCID: PMC3273836 DOI: 10.1101/gad.182980.111
Source DB: PubMed Journal: Genes Dev ISSN: 0890-9369 Impact factor: 11.361