Reversing drug resistance in vivo

Wendel, H. G., Lowe, S. W. (July 2004) Reversing drug resistance in vivo. Cell Cycle, 3 (7). pp. 847-9. ISSN 1551-4005 (Electronic)

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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 to chemotherapy-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.

Item Type: Paper
Uncontrolled Keywords: Animals Antibiotics Antineoplastic pharmacology therapeutic use Apoptosis drug effects physiology Cell Transformation Neoplastic drug effects genetics metabolism Drug Resistance Neoplasm physiology Eukaryotic Initiation Factor-4E genetics/metabolism Gene Expression Regulation Neoplastic drug effects genetics Humans Neoplasms drug therapy genetics/metabolism Protein Kinases drug effects metabolism Proto-Oncogene Proteins c-akt genetics metabolism Sirolimus pharmacology therapeutic use
Subjects: organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > apoptosis
diseases & disorders > cancer > drugs and therapies
diseases & disorders > cancer > cancer types > lymphoma
CSHL Authors:
Communities: CSHL labs > Lowe lab
Depositing User: CSHL Librarian
Date: July 2004
Date Deposited: 17 Jan 2012 17:57
Last Modified: 17 Jan 2012 17:57
URI: http://repository.cshl.edu/id/eprint/22515

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