Genomic and transcriptional aberrations linked to breast cancer pathophysiologies

Kwang-Yung Chin, Sandy DeVries, Jane Fridlyand, Paul 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 LjungLaura Esserman, Donna G. Albertson, Frederic M. Waldman, Joe Gray

Research output: Contribution to journalArticle

918 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)529-541
Number of pages13
JournalCancer Cell
Volume10
Issue number6
DOIs
Publication statusPublished - Dec 2006
Externally publishedYes

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