Abstract

Abstract Large scale characterization of cancer genomes has led to information regarding the identify, number, and types of alterations found in human tumors. However, the large number of mutations identified to date require complementary approaches to understand the function of these mutated genes and to elucidate pathways involved in cancer initiation and progression. Over the past several years, we have developed genome scale RNAi libraries and open reading frame expression libraries that permit a systematic evaluation of genes involved in cancer initiation and maintenance. We have used these tools to dissect known and novel pathways involved in malignant transformation. In particular, we have dissected the signaling pathways related to one of the most frequently mutated oncogenes KRAS, that has proven to be difficult to target therapeutically. We have identified new components of KRAS effector pathways that are essential for the survival of KRAS driven cancers. We have also developed signatures that allow us to dissect KRAS-driven gene programs that correspond to KRAS-dependence. We have used this information to develop inhibitors of components of KRAS signaling that show promise in KRAS-driven cancer models. Citation Format: William C. Hahn. Systematic functional genomics and KRAS. [abstract]. In: Proceedings of the AACR Special Conference on RAS Oncogenes: From Biology to Therapy; Feb 24-27, 2014; Lake Buena Vista, FL. Philadelphia (PA): AACR; Mol Cancer Res 2014;12(12 Suppl):Abstract nr IA08. doi: 10.1158/1557-3125.RASONC14-IA08

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