Genomic and transcriptional aberrations linked to breast cancer pathophysiologies Export

@article{citeulike:1033371, 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.}, address = {Comprehensive Cancer Center, 2340 Sutter Street, University of California, San Francisco, San Francisco, California 94143.}, author = {Chin, Koei and Devries, Sandy and Fridlyand, Jane and Spellman, Paul T. and Roydasgupta, Ritu and Kuo, Wen-Lin and Lapuk, Anna and Neve, Richard M. and Qian, Zuwei and Ryder, Tom}, citeulike-article-id = {1033371}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.ccr.2006.10.009}, citeulike-linkout-1 = {http://linkinghub.elsevier.com/retrieve/pii/S1535610806003151}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/17157792}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=17157792}, citeulike-linkout-4 = {http://www.sciencedirect.com/science/article/B6WWK-4MJBN1N-B/1/fdf1c369fd01629172d89dfab469ee2d}, doi = {10.1016/j.ccr.2006.10.009}, issn = {15356108}, journal = {Cancer Cell}, keywords = {breast\_cancer, cnv, genomics}, month = {December}, number = {6}, pages = {529--541}, posted-at = {2009-03-14 17:07:54}, priority = {2}, title = {Genomic and transcriptional aberrations linked to breast cancer pathophysiologies}, url = {http://dx.doi.org/10.1016/j.ccr.2006.10.009}, volume = {10}, year = {2006} }

TY - JOUR ID - citeulike:1033371 L3 - citeulike-article-id:1033371 N2 - 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. IS - 6 JF - Cancer Cell SN - 15356108 AD - Comprehensive Cancer Center, 2340 Sutter Street, University of California, San Francisco, San Francisco, California 94143. EP - 541 TI - Genomic and transcriptional aberrations linked to breast cancer pathophysiologies VL - 10 SP - 529 KW - breast_cancer KW - cnv KW - genomics AU - Chin, Koei AU - Devries, Sandy AU - Fridlyand, Jane AU - Spellman, Paul AU - Roydasgupta, Ritu AU - Kuo, Wen-Lin AU - Lapuk, Anna AU - Neve, Richard AU - Qian, Zuwei AU - Ryder, Tom PY - 2006/12// UR - http://dx.doi.org/10.1016/j.ccr.2006.10.009 ER -