| First Author | Glaser SP | Year | 2012 |
| Journal | Genes Dev | Volume | 26 |
| Issue | 2 | Pages | 120-5 |
| PubMed ID | 22279045 | Mgi Jnum | J:179881 |
| Mgi Id | MGI:5304579 | Doi | 10.1101/gad.182980.111 |
| Citation | Glaser SP, et al. (2012) Anti-apoptotic Mcl-1 is essential for the development and sustained growth of acute myeloid leukemia. Genes Dev 26(2):120-5 |
| abstractText | 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. |
