Richard Marais

Education Marais was educated at University College London where he was awarded a Bachelor of Science degree in Genetics and Microbiology in 1985. He completed his postgraduate study at the Ludwig Institute for Cancer Research and was awarded a PhD in 1989 for research on isotypes of the protein kinase C (PKC) enzyme supervised by Peter Parker.

Career and research Marais's research investigates the biology of melanoma and other cancers in order to deliver better treatment strategies for patients. and cell signalling significantly advanced understanding of melanoma biology and aetiology. He translated his basic research discoveries into clinical implementation, improving patient outcomes, elucidating mechanisms of drug resistance and developing new drugs against BRAF and other cancer targets.

Awards and honours With colleagues, Marais received the American Association for Cancer Research (AACR) Team Science Award in 2012 for cancer drug discoveries. He was elected a member of the European Molecular Biology Organization (EMBO) in 2009, His citation on election reads: centered Richard Marais is Professor of Molecular Oncology at Cancer Research UK and has made important contributions to the understanding of cell signalling pathways, particularly in cancer. He was amongst the first to show that mitogen activated protein kinases regulate gene expression by directly phosphorylating transcription factors. However his greatest impact has been with the RAF kinase family, where he discovered that individual RAF proteins are regulated differentially and shown how they respond to RAS, which is mutated in a third of all human tumours. He was a key member of the team that demonstrated that B-RAF is encoded by an oncogene, which is a culprit in most human melanomas. He went on to validate B-RAF as a therapeutic target. In collaboration with David Barford, he solved the crystal structure of B-RAF and explained how it is activated by mutations that occur in cancer. He elucidated why C-RAF is not mutated in cancer, showing that mutant forms of B-RAF can activate C-RAF through a novel mechanism, establishing a new paradigm of RAF signaling. He is now translating these studies to the clinic by leading a large effort to design and synthesize new anti-B-RAF drugs that will be used to treat melanoma.