Author/Authors :
Neve، نويسنده , , Richard M. and Chin، نويسنده , , Koei and Fridlyand، نويسنده , , Jane and Yeh، نويسنده , , Jennifer and Baehner، نويسنده , , Frederick L. and Fevr، نويسنده , , Tea and Clark، نويسنده , , Laura and Bayani، نويسنده , , Nora and Coppe، نويسنده , , Jean-Philippe and Tong، نويسنده , , Frances and Speed، نويسنده , , Terry and Spellman، نويسنده , , Paul T. and DeVries، نويسنده , , Sandy and Lapuk، نويسنده , , Anna and Wang، نويسنده , , Nick J. and Kuo، نويسنده , , Wen-Lin and Stilwell، نويسنده , , Jackie L. and Pinkel، نويسنده , , Daniel and Albertson، نويسنده , , Donna G. and Waldman، نويسنده , , Frederic M. and McCormick، نويسنده , , Frank and Dickson، نويسنده , , Robert B. and Johnson، نويسنده , , Michael D. and Lippman، نويسنده , , Marc and Ethier، نويسنده , , Stephen and Gazdar، نويسنده , , Adi and Gray، نويسنده , , Joe W.، نويسنده ,
Abstract :
Summary
studies suggest that thousands of genes may contribute to breast cancer pathophysiologies when deregulated by genomic or epigenomic events. Here, we describe a model “system” to appraise the functional contributions of these genes to breast cancer subsets. In general, the recurrent genomic and transcriptional characteristics of 51 breast cancer cell lines mirror those of 145 primary breast tumors, although some significant differences are documented. The cell lines that comprise the system also exhibit the substantial genomic, transcriptional, and biological heterogeneity found in primary tumors. We show, using Trastuzumab (Herceptin) monotherapy as an example, that the system can be used to identify molecular features that predict or indicate response to targeted therapies or other physiological perturbations.
