Genomic and transcriptional aberrations linked to breast cancer pathophysiologies

Koei Chin, 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 LjungLaura Esserman, Donna G. Albertson, Frederic M. Waldman, Joe W. Gray

Research output: Contribution to journalArticlepeer-review


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
Issue number6
StatePublished - Dec 2006



ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research


Dive into the research topics of 'Genomic and transcriptional aberrations linked to breast cancer pathophysiologies'. Together they form a unique fingerprint.

Cite this