Karen H. Vousden
The Francis Crick Institute
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Primary Section: 41, Medical Genetics, Hematology, and Oncology Membership Type:
International Member
(elected 2018)
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Biosketch
Karen Vousden is a cancer biologist recognized for her work on the regulation and function of the p53 tumour suppressor protein. Karen was born and raised in Gravesend, UK. She graduated from the University of London with a BSc in Genetics and Microbiology and a PhD in Genetics. Following postdoctoral fellowships at the Institute of Cancer Research in London and the National Cancer Institute in Maryland, Karen took up a faculty positions at the Ludwig Institute for Cancer Research in London and the National Cancer Institute, before taking the post of Director of the Beatson Institute in Glasgow. Finally, she returned to London to join the Francis Crick Institute and become Chief Scientist for Cancer Research UK. Karen has been elected as a Fellow of the Royal Society, the Royal Society of Edinburgh, the Academy of Medical Sciences, EMBO, the European Academy of Sciences, the American Association of Cancer Research and the American Academy of Arts and Sciences. She was made a Commander of the British Empire for services to clinical science.
Research Interests
p53 is a tumor suppressor protein that is mutated or dysfunctional in most cancers. Karen’s laboratory has focused on understanding how p53 is controlled and how it functions to limit malignant progression. They contributed to the discovery that MDM2 promotes the ubiquitin-dependent degradation of p53, identifying MDM2 as a therapeutic target that has been developed into new drugs currently in clinical trials. Karen’s group was also one that identified the BH3 domain protein PUMA as a key mediator of p53-induced death and more recently they have elucidated mechanisms through which p53 modulates metabolism and supports adaptation to nutrient stress. This work has revealed an unexpected ability of p53 to help cells adapt and survive under transient periods of nutrient starvation. Finally, Karen’s group showed that tumor derived p53 mutants acquire an ability to drive invasion and metastasis through a mechanism that involves the recycling of cell surface receptors. Many human cancers express mutant p53 and the therapeutic implications of these observations are now under investigation.
