乳腺癌
表观遗传学
生物
癌症
曲妥珠单抗
计算生物学
癌症研究
基因
生物信息学
遗传学
DNA甲基化
基因表达
作者
Richard M. Neve,Koei Chin,Jane Fridlyand,Jennifer Yeh,Frederick L. Baehner,Tea Fevr,Laura Ashley Clark,Nora Bayani,Jean‐Philippe Coppé,Frances Tong,Terence P. Speed,Paul T. Spellman,Sandy DeVries,Anna Lapuk,N. Wang,Wen‐Lin Kuo,Jackie L. Stilwell,Daniel Pinkel,Donna G. Albertson,Frederic M. Waldman
出处
期刊:Cancer Cell
[Cell Press]
日期:2006-12-01
卷期号:10 (6): 515-527
被引量:3110
标识
DOI:10.1016/j.ccr.2006.10.008
摘要
Summary Recent 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.
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