| Literature DB >> 17157792 |
Koei Chin1, Sandy DeVries, Jane Fridlyand, Paul T Spellman, Ritu Roydasgupta, Wen-Lin Kuo, Anna Lapuk, Richard M Neve, Zuwei Qian, Tom Ryder, Fanqing Chen, Heidi Feiler, Taku Tokuyasu, Chris Kingsley, Shanaz Dairkee, Zhenhang Meng, Karen Chew, Daniel Pinkel, Ajay Jain, Britt Marie Ljung, Laura Esserman, Donna G Albertson, Frederic M Waldman, Joe W Gray.
Abstract
This study explores the roles of genome copy number abnormalities (CNAs) in breast cancer pathophysiology by identifying associations between recurrent CNAs, gene expression, and clinical outcome in a set of aggressively treated early-stage breast tumors. It shows that the recurrent CNAs differ between tumor subtypes defined by expression pattern and that stratification of patients according to outcome can be improved by measuring both expression and copy number, especially high-level amplification. Sixty-six genes deregulated by the high-level amplifications are potential therapeutic targets. Nine of these (FGFR1, IKBKB, ERBB2, PROCC, ADAM9, FNTA, ACACA, PNMT, and NR1D1) are considered druggable. Low-level CNAs appear to contribute to cancer progression by altering RNA and cellular metabolism.Entities:
Mesh：
Year: 2006 PMID： 17157792 DOI： 10.1016/j.ccr.2006.10.009
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743