Mutations of the BRAF gene in human cancer

@article{Davies2002MutationsOT,
  title={Mutations of the BRAF gene in human cancer},
  author={H. Davies and G. Bignell and Charles Cox and P. Stephens and S. Edkins and S. Clegg and J. Teague and H. Woffendin and M. Garnett and W. Bottomley and Neil Davis and E. Dicks and Rebecca Ewing and Yvonne Floyd and K. Gray and S. Hall and R. Hawes and Jaime Hughes and V. Kosmidou and A. Menzies and Catherine Mould and A. Parker and C. Stevens and S. Watt and S. Hooper and Rebecca Wilson and H. Jayatilake and B. Gusterson and C. Cooper and J. Shipley and D. Hargrave and K. Pritchard-Jones and N. Maitland and G. Chenevix-Trench and G. Riggins and D. Bigner and G. Palmieri and A. Cossu and A. Flanagan and A. Nicholson and J. Ho and S. Leung and S. Yuen and B. Weber and H. Seigler and T. Darrow and H. Paterson and R. Marais and C. Marshall and R. Wooster and M. Stratton and P. Futreal},
  journal={Nature},
  year={2002},
  volume={417},
  pages={949-954}
}
Cancers arise owing to the accumulation of mutations in critical genes that alter normal programmes of cell proliferation, differentiation and death. As the first stage of a systematic genome-wide screen for these genes, we have prioritized for analysis signalling pathways in which at least one gene is mutated in human cancer. The RAS–RAF–MEK–ERK–MAP kinase pathway mediates cellular responses to growth signals. RAS is mutated to an oncogenic form in about 15% of human cancer. The three RAF… Expand
Sequencing analysis of BRAF mutations in human cancers.
Mutations of the BRAF gene in human cancer, by Davies et al. (Nature 2002; 417: 949–54)
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