Reversing Drug Resistance In Vivo
- 1 July 2004
- journal article
- review article
- Published by Taylor & Francis in Cell Cycle
- Vol. 3 (7) , 845-847
- https://doi.org/10.4161/cc.3.7.976
Abstract
Apoptotic defects occur in oncogenesis and contribute to drug resistance. We have shown that Bcl-2, Akt, and the translational regulator eIF4E cooperate with Myc during lymphomagenesis and are potent inducers of drug resistance. Interestingly, lymphomas expressing Akt, but not those expressing Bcl-2 are sensitized tochemotherapy-induced apoptosis by the mTOR inhibitor rapamycin, an effect that is countered by eIF4E. These results provide in vivo validation for a strategy to reverse drug resistance in human cancers and highlight the potential role of translational deregulation in oncogenesis and resistance. They also illustrate the importance of tailoring cancer therapy based on tumor genotype.Keywords
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