Frank McCormick
University of California, San Francisco
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Primary Section: 41, Medical Genetics, Hematology, and Oncology Membership Type:
Member
(elected 2014)
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Biosketch
Frank McCormick, PhD, FRS, DSc (Hon) is the Professor Emeritus of the University of California, San Francisco (UCSF) Helen Diller Family Comprehensive Cancer Center. A native of Cambridge, England, Dr. McCormick received his BSc in biochemistry from the University of Birmingham (1972) and his PhD in biochemistry from the University of Cambridge (1975). Postdoctoral fellowships were held at the State University of New York at Stony Brook and in London at the Imperial Cancer Research Fund. He has been a Fellow of the Royal Society since 1996 and a Member of the National Academy of Sciences since 2014. Prior to joining the UCSF faculty, Dr. McCormick pursued cancer-related work at Cetus Corporation (Director of Molecular Biology, 1981-90; Vice President of Research, 1990-91) and Chiron Corporation, (Vice President of Research from 1991-92) and in 1992 he founded Onyx Pharmaceuticals and served as its Chief Scientific Officer until 1996. His group discovered and developed sorafenib and palbociclib, and pioneered cancer therapy using oncolytic viruses. His laboratory at UCSF focuses on functions of Ras proteins. More recently, he has taken a leadership role at the Frederick National Laboratory for Cancer Research, overseeing an NCI supported national effort to develop therapies against Ras-driven cancers.
Research Interests
Frank McCormick’s lab is devoted to basic Ras discovery science and focuses on identifying new ways of treating disease driven by Ras proteins. They have identified the molecular basis of the effects in which K-Ras proteins promote stem-cell properties in cancer cells, enable them to establish metastatic tumors with high efficiency, and become drug resistant. The McCormick lab has identified small molecules that binds irreversibly to K-Ras and prevent prenylation. Another challenge they are tackling is the crystal structure of the K-Ras protein in hopes that any discovery could provide a new and safe way of blocking K-Ras function. With a developed collection of highly potent and specific siRNAs that target K-Ras and the components of the pathways, combinations of these siRNAs have resulted tumor destruction in vivo. They developed a system of expressing single Ras isoforms in a “Ras-less” MEF background as a discovery tool to identify specific biochemical properties of individual Ras proteins in a clean background. Additionally, major progress has been made in understanding the mechanism underlying Neurofibromatosis Type 1 (NF1). The gene responsible for NF1 encodes a protein that negatively regulates Ras and loss of the gene results in hyperactivation of Ras. The NF1 protein depends on another protein, SPRED1, which is mutated in another familial syndrome called Legius Syndrome.
