Author/Authors :
Chin، نويسنده , , Koei and DeVries، نويسنده , , Sandy and Fridlyand، نويسنده , , Jane and Spellman، نويسنده , , Paul T. and Roydasgupta، نويسنده , , Ritu and Kuo، نويسنده , , Wen-Lin and Lapuk، نويسنده , , Anna and Neve، نويسنده , , Richard M. and Qian، نويسنده , , Zuwei and Ryder، نويسنده , , Tom and Chen، نويسنده , , Fanqing and Feiler، نويسنده , , Heidi and Tokuyasu، نويسنده , , Taku and Kingsley، نويسنده , , Chris and Dairkee، نويسنده , , Shanaz and Meng، نويسنده , , Zhenhang and Chew، نويسنده , , Karen and Pinkel، نويسنده , , Daniel and Jain، نويسنده , , Ajay and Ljung، نويسنده , , Britt Marie and Esserman، نويسنده , , Laura and Albertson، نويسنده , , Donna G. and Waldman، نويسنده , , Frederic M. and Gray، نويسنده , , Joe W.، نويسنده ,
Abstract :
Summary
tudy 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.
