Authors:
Philip J. Stephens, Patrick S. Tarpey, Helen Davies, Peter Van Loo, Chris Greenman, David C. Wedge, Serena Nik Zainal, Sancha Martin, Ignacio Varela, Graham R. Bignell, Lucy R. Yates, Elli Papaemmanuil, David Beare, Adam Butler, Angela Cheverton, John Gamble, Jonathan Hinton, Mingming Jia, Alagu Jayakumar, David Jones, Calli Latimer, King Wai Lau, Stuart McLaren, David J. McBride, Andrew Menzies, Laura Mudie, Keiran Raine, Roland Rad, Michael Spencer Chapman, Jon Teague, Douglas Easton, Anita Langerød, OSBREAC, Ming Ta Michael Lee, Chen-Yang Shen, Benita Tan Kiat Tee, Bernice Wong Huimin, Annegien Broeks, Ana Cristina Vargas, Gulisa Turashvili, John Martens, Aquila Fatima, Penelope Miron, Suet-Feung Chin, Gilles Thomas, Sandrine Boyault, Odette Mariani, Sunil R. Lakhani, Marc van de Vijver, Laura van ‘t Veer, John Foekens, Christine Desmedt, Christos Sotiriou, Andrew Tutt, Carlos Caldas, Jorge S. Reis-Filho, Samuel A. J. R. Aparicio, Anne Vincent Salomon, Anne-Lise Børresen-Dale, Andrea Richardson, Peter J. Campbell, P. Andrew Futreal, Michael R. Stratton, Rolf Karesen, Ellen Schlichting, Bjorn Naume, Torill Sauer, & Lars Ottestad for The Oslo Breast Cancer Consortium (OSBREAC)
Summary:
All cancers carry somatic mutations in their genomes. A subset, known as driver mutations, confer clonal selective advantage on cancer cells and are causally implicated in oncogenesis1, and the remainder are passenger mutations. The driver mutations and mutational processes operative in breast cancer have not yet been comprehensively explored. Here…
Source:
Nature; (05/16/12)