| Literature DB >> 15457249 |
Philip Stephens1, Chris Hunter, Graham Bignell, Sarah Edkins, Helen Davies, Jon Teague, Claire Stevens, Sarah O'Meara, Raffaella Smith, Adrian Parker, Andy Barthorpe, Matthew Blow, Lisa Brackenbury, Adam Butler, Oliver Clarke, Jennifer Cole, Ed Dicks, Angus Dike, Anja Drozd, Ken Edwards, Simon Forbes, Rebecca Foster, Kristian Gray, Chris Greenman, Kelly Halliday, Katy Hills, Vivienne Kosmidou, Richard Lugg, Andy Menzies, Janet Perry, Robert Petty, Keiran Raine, Lewis Ratford, Rebecca Shepherd, Alexandra Small, Yvonne Stephens, Calli Tofts, Jennifer Varian, Sofie West, Sara Widaa, Andrew Yates, Francis Brasseur, Colin S Cooper, Adrienne M Flanagan, Margaret Knowles, Suet Y Leung, David N Louis, Leendert H J Looijenga, Bruce Malkowicz, Marco A Pierotti, Bin Teh, Georgia Chenevix-Trench, Barbara L Weber, Siu T Yuen, Grace Harris, Peter Goldstraw, Andrew G Nicholson, P Andrew Futreal, Richard Wooster, Michael R Stratton.
Abstract
The protein-kinase family is the most frequently mutated gene family found in human cancer and faulty kinase enzymes are being investigated as promising targets for the design of antitumour therapies. We have sequenced the gene encoding the transmembrane protein tyrosine kinase ERBB2 (also known as HER2 or Neu) from 120 primary lung tumours and identified 4% that have mutations within the kinase domain; in the adenocarcinoma subtype of lung cancer, 10% of cases had mutations. ERBB2 inhibitors, which have so far proved to be ineffective in treating lung cancer, should now be clinically re-evaluated in the specific subset of patients with lung cancer whose tumours carry ERBB2 mutations.Entities:
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Year: 2004 PMID： 15457249 DOI： 10.1038/431525b
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962