Abstract

Abstract Cancer is a multistep Darwinian process whereby mutant cells able to escape internal, environmental, or drug-mediated proliferative roadblocks expand and outcompete less-fit cells. Mutations characterizing this somatic evolution range from single-point mutations to whole-chromosome aneuploidy. Although sequence mutations clearly play a role in cancer evolution, the role of aneuploidy in cancer is far less clear. Previously, we investigated how yeast cells can adapt in response to a proliferative roadblock and the role of aneuploidy during this process. We showed that aneuploidy could provide a source of heritable variation driving the emergence of large phenotypic changes that can be adaptive under strong selective conditions. Recently, we provided evidence that aneuploidy is sufficient to generate global changes at the proteome level and to provide phenotypic variation. Taken together, our data suggest that aneuploidy might thus be beneficial to cancer cells that are trying to escape growth inhibitory signals and chemotherapy treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr C57.

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