| Autor: |
Glaser SP; The Walter and Eliza Hall Institute, Parkville, Melbourne, Victoria 3052, Australia., Lee EF, Trounson E, Bouillet P, Wei A, Fairlie WD, Izon DJ, Zuber J, Rappaport AR, Herold MJ, Alexander WS, Lowe SW, Robb L, Strasser A |
| Jazyk: |
angličtina |
| Zdroj: |
Genes & development [Genes Dev] 2012 Jan 15; Vol. 26 (2), pp. 120-5. |
| DOI: |
10.1101/gad.182980.111 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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