Richard Marais

Molecular Oncology at the University of Manchester.^[2][9]

PhD in 1989 for research on isotypes of the protein kinase C (PKC) enzyme supervised by Peter Parker.^[5]

aetiology.^[2][11] 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.^[2] His research informs innovative clinical trial designs with signal-seeking biomarkers to monitor therapy responses and optimise patient treatment.^[2] His research also highlights the importance of combining sunscreen with other sun avoidance strategies to reduce population melanoma risk.^[2]

c-Fos.^[8]

Institute of Cancer Research (ICR), after which Marais set up his own laboratory in 1998 before moving to Manchester in 2012.^[6]

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.^[7]