Genomic and transcriptional aberrations linked to breast cancer pathophysiologies - PubMed (original) (raw)

doi: 10.1016/j.ccr.2006.10.009.

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

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Genomic and transcriptional aberrations linked to breast cancer pathophysiologies

Koei Chin et al. Cancer Cell. 2006 Dec.

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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.

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