NOV 29, 2017 10:00 AM PST

WEBINAR: RAS Oncoproteins: Therapeutic Vulnerabilities

C.E. CREDITS: P.A.C.E. CE | Florida CE
  • Associate Professor of Radiation Oncology and Pharmacology, University of North Carolina at Chapell Hill
      Adrienne D. Cox, PhD, is Chief of the Division of Cancer Research in the Department of Radiation Oncology at the University of North Carolina at Chapel Hill (UNC-CH), Associate Professor of Pharmacology, and a member of the Lineberger Comprehensive Cancer Center (LCCC), where she directs UNC-CH's NCI-funded Cancer Cell Biology T32 Training Program. Dr. Cox serves on numerous internal and external mentoring committees and grant review panels, reviewing for the National Cancer Institute (NCI) as well as nonprofit organizations such as the American Cancer Society and the Pancreatic Cancer Action Network. She received her BA from Pomona College, her PhD from Eastern Virginia Medical School, and performed her postdoctoral studies at the La Jolla Cancer Research Foundation (now the Sanford Burnham Prebys Medical Discovery Institute). She has been involved in the study of RAS proteins since the discovery of their lipid modification by prenylation, publishing over 100 articles in peer-reviewed journals and consulting over the years for numerous pharmaceutical companies. Dr. Cox's research encompasses basic science aspects of RAS family signaling and transformation as well as translational aspects such as the development of farnesyltransferase inhibitors, originally intended to be anti-RAS therapeutics. Her laboratory is a constituent of the RAS Synthetic Lethal Network, a component of NCI's RAS Initiative that seeks to identify and target RAS therapeutic vulnerabilities.


    DATE: November 29, 2017
    TIME: 10:00 AM PST

    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.

    Learning Objectives:

    • Understand RAS function in cytoplasmic signaling
    • Understand the  potential therapeutic role of anti-RAS therapy in Cancer

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