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Nature 462, 44-45 (5 November 2009) | doi:10.1038/462044a; Published online 4 November 2009
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Postdoctoral Fellow - Computational Genomics - Team 78 – Ref: 80464
- Wellcome Trust Sanger Institute
- Hinxton, Cambridgeshire CB10 1, UK
Leadership Fellowships
- University of Oxford
- Oxford United Kingdom
Cancer: A tumour gene's fatal flaws
Julian Downward1
Abstract
Mutations in RAS genes are common in human tumours, but RAS has proved impossible to target with drugs. Its associated NF-
B signalling pathway, however, may turn out to be this tumour gene's Achilles heel.
RAS is one of the most commonly mutated gene families in human cancers — one of its three members (KRAS, HRAS and NRAS) is mutated in about 20% of human tumours. Attempts to target mutant RAS proteins directly with small-molecule inhibitors have so far proved unsuccessful, so there has been considerable interest in finding signalling pathways that function downstream of RAS and whose blockade might be selectively toxic to tumour cells.
- Julian Downward is at Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.
Email: downward@cancer.org.uk
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