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Gerard I. EvanGerard I. Evan Ph.D., FRS Gerard Evan “grew up” in London, UK and received his MA in Biochemistry from the University of Oxford in 1977. He then moved to the Medical Research Council (MRC) Laboratory of Molecular Biology at the University of Cambridge where he gained a PhD in Molecular Immunology in 1981 using monoclonal antibodies to define immunological targets on tumor cells. He was first an MRC Traveling Fellow and later a UK Science Research Council Post-Doctoral Fellow in the laboratory of J. Michael Bishop at UCSF from 1982-84. There he developed an abiding interest in the molecular mechanisms of cell growth and cell death, focusing particularly on elucidating the biology of the enigmatic Myc protein, a powerful engine of cell proliferation that is aberrantly expressed in most human cancers. In 1988 he was recruited to the Imperial Cancer Research Fund (ICRF) Laboratories in London, appointed Napier Professor of the Royal Society in 1996, and in 1999 appointed to the Gerson and Barbara Bass Bakar Distinguished Professor of Cancer Biology, joining the faculty of the UCSF Cancer Center. In 2001, Dr Evan was the Eppley Visiting Professor of Cancer Research at the University of Nebraska, Omaha and a visiting Professor of the Norwegian Academy of Sciences; in 2002 he was visiting professor at the European Cancer Genetics School in Italy and, in 2003, visiting professor at the National University of Singapore. He was elected a member of the European Molecular Biology Organization in 1996, a Fellow of the UK Academy of Medical Sciences in 1999 and a fellow of the Royal Society of London in 2004. Dr Evan’s research is focused on understanding the processes responsible for genesis and maintenance of cancers, in particular cancers of the pancreas, colon, brain, skin and liver. In 1992, he made the unexpected and counter-intuitive discovery that mutations that drive cancer cell proliferation also drive the contradictory pathway of cell suicide and proposed that this coupling of opposing pathways is a central innate tumor suppressive mechanism built into all human cells. Only when this coupling fails can cancers emerge and, by inference, re-instatement of the defective cell suicide pathway would lead to the rapid and specific demise of cancer cells. Understanding the molecular mechanisms that underlie the cell suicide machinery and how it can be manipulated therapeutically are the overarching aims of his laboratory. |
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