Adrienne Cox, Ph.D. Associate Professor, UNC Chapel Hill
The three human RAS↗ genes (HRAS↗, KRAS↗ and NRAS↗) encode four highly related RAS small GTPases↗ (HRAS, KRAS4A, KRAS4B and NRAS). RAS proteins function as GDP-GTP regulated binary on-off switches that regulate diverse cytoplasmic signaling networks. In cancer and developmental disorders (RASopathies), mutationally activated RAS proteins drive aberrant signal transduction. RAS proteins are also the founding members of a large superfamily of small GTPases comprised of >150 members. Since their initial identification decades ago as drivers of human cancers, there has been intense interest and effort in targeting RAS for cancer treatment. RAS genes are the most frequently mutated oncogenes in the top three causes of cancer deaths in the US in 2016 (lung, colorectal and pancreatic cancers). In this webinar, I will discuss the vulnerabilities of RAS that have been exploited for the development of pharmacologic inhibitors of RAS function.