Mutations of the BRAF gene in human cancer (Articolo in rivista)

Type
Label
  • Mutations of the BRAF gene in human cancer (Articolo in rivista) (literal)
Anno
  • 2002-01-01T00:00:00+01:00 (literal)
Alternative label
  • Davies H, Bignell GR., Cox C., Stephens P., Edkins S., Clegg S., Teague J., Woffendin H, Garnett M.J., Bottomley W, Davis N., Dicks E., Ewing R., Hargrave D., Pritchard-Jones K, Maitland N., Chenevix-Trench G., Riggins GJ., Bigner D.D, Palmieri G., Cossu (2002)
    Mutations of the BRAF gene in human cancer
    in Nature (Lond.)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Davies H, Bignell GR., Cox C., Stephens P., Edkins S., Clegg S., Teague J., Woffendin H, Garnett M.J., Bottomley W, Davis N., Dicks E., Ewing R., Hargrave D., Pritchard-Jones K, Maitland N., Chenevix-Trench G., Riggins GJ., Bigner D.D, Palmieri G., Cossu (literal)
Pagina inizio
  • 949 (literal)
Pagina fine
  • 954 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 417 (literal)
Rivista
Note
  • PubMed (literal)
  • ISI Web of Science (WOS) (literal)
  • Scopus (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Cancer Genome Project, The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, CB10 1SA, UK Cancer Research UK Centre for Cell and Molecular Biology, Chester Beatty Labs, Institute of Cancer Research, London SW3 6JB, UK Section of Cancer Genetics; Section of Molecular Carcinogenesis; and Section of Paediatrics, Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK Department of Pathology, Western Infirmary, University of Glasgow, S11 6NT,UK Department of Biology, YCR Cancer Research Unit, University of York, York YO10 5YW, UK Queensland Institute of Medical Research, RBH Post Office Herston, Queensland 4029, Australia Department of Pathology, andDepartment of Surgery, Duke University Medical Centre, Durham, North Carolina 27710, USA Institute of Molecular Genetics, C.N.R., Loc. Tramariglio, Alghero 07040, Italy Department of Pathology, University of Sassari, Azienda USL1, Sassari 07100,Italy Royal Free & University College Medical School, London WC1E 6JJ, UK Royal Brompton Hospital, London SW3 6NP, UK Department of Surgery, and Department of Pathology, The University of Hong Kong, Queen Mary Hospital, Hong Kong Abramson Family Cancer Research Institute, University of Pennsylvania Cancer Center, Philadelphia, Pennsylvania 19104, USA (literal)
Titolo
  • Mutations of the BRAF gene in human cancer (literal)
Abstract
  • 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 genomewide 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 signals1. RAS is mutated to an oncogenic formin about 15% of human cancer. The three RAF genes code for cytoplasmic serine/threonine kinases that are regulated by binding RAS1–3. Here we report BRAF somatic missense mutations in 66% of malignant melanomas and at lower frequency in a wide range of human cancers. All mutations are within the kinase domain, with a single substitution (V599E) accounting for 80%.Mutated BRAF proteins have elevated kinase activity and are transforming in NIH3T3 cells. Furthermore, RAS function is not required for the growth of cancer cell lines with the V599E mutation. As BRAF is a serine/threonine kinase that is commonly activated by somatic point mutation in human cancer, it may provide new therapeutic opportunities in malignant melanoma (literal)
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