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• W1973001092 abstract "Deregulated Myc expression drives many human cancers, including Burkitt's lymphoma and a highly aggressive subset of diffuse large cell lymphomas. Myc-driven tumors often display resistance to chemotherapeutics because of acquisition of mutations that impair the apoptosis pathway regulated by the Bcl-2 protein family. Given the need to identify new therapies for such lymphomas, we have evaluated the efficacy of ABT-737, a small molecule that mimics the action of the BH3-only proteins, natural antagonists of the prosurvival Bcl-2 proteins. ABT-737 selectively targets certain prosurvival proteins (Bcl-2, Bcl-x L , and Bcl-w) but not others (Mcl-1 and A1). We treated mice transplanted with lymphomas derived either from Eμ- myc transgenic mice or Eμ- myc mice that also expressed an Eμ- bcl -2 transgene. As a single agent, ABT-737 significantly prolonged the survival of mice transplanted with the myc / bcl -2 lymphomas but was ineffective for the myc lymphomas, probably because of the relatively higher Mcl-1 levels found in the latter. Strikingly, when combined with low-dose cyclophosphamide, ABT-737 produced sustained disease-free survival of all animals transplanted with two of three myc / bcl -2 lymphomas tested. The combination therapy was also more effective against some myc lymphomas than treatment with either agent alone. Our data suggest that antagonism of Bcl-2 with small organic compounds is an attractive approach to enhance the efficacy of conventional therapy for the treatment of Myc-driven lymphomas that over-express this prosurvival molecule." @default.
• W1973001092 created "2016-06-24" @default.
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• W1973001092 date "2008-11-18" @default.
• W1973001092 modified "2023-10-16" @default.
• W1973001092 title "In vivo efficacy of the Bcl-2 antagonist ABT-737 against aggressive Myc-driven lymphomas" @default.
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• W1973001092 doi "https://doi.org/10.1073/pnas.0809957105" @default.
• W1973001092 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2582212" @default.
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