Anti-apoptotic mcl-1 is essential for the development and sustained growth of acute myeloid leukemia

Glaser, S. P., Lee, E. F., Trounson, E., Bouillet, P., Wei, A., Fairlie, W. D., Izon, D. J., Zuber, J., Rappaport, A. R., Herold, M. J., Alexander, W. S., Lowe, S. W., Robb, L., Strasser, A. (January 2012) Anti-apoptotic mcl-1 is essential for the development and sustained growth of acute myeloid leukemia. Genes and Development, 26 (2). pp. 120-125. ISSN 08909369 (ISSN)

URL: http://www.ncbi.nlm.nih.gov/pubmed/22279045
DOI: 10.1101/gad.182980.111

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.

Item Type: Paper
Subjects: diseases & disorders > cancer
diseases & disorders
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions
organs, tissues, organelles, cell types and functions > cell types and functions
diseases & disorders > cancer > cancer types > leukemia
diseases & disorders > cancer > cancer types
CSHL Authors:
Communities: CSHL Cancer Center Shared Resources > Animal Services
CSHL Cancer Center Shared Resources > DNA Sequencing Service
CSHL Cancer Center Shared Resources > Flow Cytometry Service
CSHL labs > Lowe lab
Watson School > Publications
CSHL Cancer Center Program > Cancer Genetics
Depositing User: Matt Covey
Date: January 2012
Date Deposited: 30 Jan 2013 21:59
Last Modified: 14 Oct 2015 16:24
PMCID: PMC3273836
Related URLs:
URI: http://repository.cshl.edu/id/eprint/26950

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