The largest survey yet of the human genome in cancer, published in 'Nature' this month, shows that the number of mutated genes driving development of cancer is greater than previously thought.

Scientists at the Wellcome Trust Sanger Institute sequenced more than 500 'kinase' genes in 210 cancers, including breast, lung, colorectal and stomach cancers, to gain new insights into how the cancers develop.

All cancers are believed to be due to mutations – abnormalities in genes. Led by Professor Mike Stratton and Dr Andy Futreal, co-leaders of the Cancer Genome Project at the Sanger Institute, the researchers found more than 1000 mutations in the kinase genes, and divided the mutations into 'drivers' and 'passengers'.

Driver mutations are the ones that cause cancer cells to grow, while 'passengers', mutations that have hitchhiked along for the ride, make no contribution to cancer development. The research team identified possible driver mutations in 120 genes, most of which had not been seen before.

The new research suggests that many more genes are involved in cancer development than previously realised. Identifying these genes and mutations is crucial for diagnosis and to develop accurately targeted treatments.

Kinase proteins are interesting as they can act as a series of relays, switching on and off in our cells, controlling cell behaviour (such as cell division). One example is the BRAF gene: the 2002 pilot phase of the team's work showed that BRAF was mutated in more than 60 per cent of cases of malignant melanoma. That observation has driven discovery of new drugs to treat melanoma, some of which are in clinical trials.

See also

• A gene for skin cancer

External links

• Drivers and Passengers on the Road to Cancer (Sanger Institute press release, 7 March 2007)
• Greenman C et al. Patterns of somatic mutation in human cancer genomes. Nature 2007;446:153-8.
• Haber DA and Settleman J. Cancer: drivers and passengers. Nature 2007;446:145-6.
• Cancer Genome Project
• COSMIC database of cancer mutations