| Literature DB >> 17157791 |
Richard M Neve1, Koei Chin, Jane Fridlyand, Jennifer Yeh, Frederick L Baehner, Tea Fevr, Laura Clark, Nora Bayani, Jean-Philippe Coppe, Frances Tong, Terry Speed, Paul T Spellman, Sandy DeVries, Anna Lapuk, Nick J Wang, Wen-Lin Kuo, Jackie L Stilwell, Daniel Pinkel, Donna G Albertson, Frederic M Waldman, Frank McCormick, Robert B Dickson, Michael D Johnson, Marc Lippman, Stephen Ethier, Adi Gazdar, Joe W Gray.
Abstract
Recent studies suggest that thousands of genes may contribute to breast cancer pathophysiologies when deregulated by genomic or epigenomic events. Here, we describe a model "system" to appraise the functional contributions of these genes to breast cancer subsets. In general, the recurrent genomic and transcriptional characteristics of 51 breast cancer cell lines mirror those of 145 primary breast tumors, although some significant differences are documented. The cell lines that comprise the system also exhibit the substantial genomic, transcriptional, and biological heterogeneity found in primary tumors. We show, using Trastuzumab (Herceptin) monotherapy as an example, that the system can be used to identify molecular features that predict or indicate response to targeted therapies or other physiological perturbations.Entities:
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Year: 2006 PMID： 17157791 PMCID： PMC2730521 DOI： 10.1016/j.ccr.2006.10.008
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743