Abstract 207: Distinct TRAIL resistance mechanisms can be overcome by proteosome inhibition
| Autor: | Christina Menke, Jacqueline Thorburn, Kian Behbakht, Lianghua Bin, Andrew Thorburn, Heide L. Ford |
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| Rok vydání: | 2010 |
| Předmět: | |
| Zdroj: | Cancer Research. 70:207-207 |
| ISSN: | 1538-7445 0008-5472 |
| DOI: | 10.1158/1538-7445.am10-207 |
| Popis: | A major impediment to the use of Tumor Necrosis Factor-Like Apoptosis Inducing Ligand (TRAIL) Receptor targeted drugs is that many tumors evolve resistance to these agents. On the other hand however, multiple different kinds of drugs are reported to be able to synergize with TRAIL. This raises the question of whether it is possible to overcome resistance using the same drugs that cause synergy. We tested this idea by creating a series of isogenic tumor cells with acquired TRAIL resistance or defined mechanisms of resistance that are known to occur in human tumors then compared these cells to the TRAIL-sensitive parental cell line. Although diverse classes of anti-cancer drug were all able to synergize with TRAIL most of these agents were unable to overcome resistance and there was no correlation between the amount of synergy that is seen with a particular agent and its ability to overcome acquired resistance. Proteosome inhibitors were however able to overcome diverse resistance mechanisms suggesting that one should select drugs for TRAIL R agonist combination therapy based not just on their ability to synergize but rather on their ability to both overcome resistance and synergy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 207. |
| Databáze: | OpenAIRE |
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