A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes

by: Richard M Neve, Koei Chin, Jane Fridlyand, Jennifer Yeh, Frederick L Baehner, Tea Fevr, Laura Clark, Nora Bayani, Jean-Philippe Coppe, Frances Tong

Cancer Cell, Vol. 10, No. 6. (December 2006), pp. 515-527.

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Abstract

SummaryRecent 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.

@article{citeulike:989152, abstract = {SummaryRecent 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.}, author = {Neve, Richard M. and Chin, Koei and Fridlyand, Jane and Yeh, Jennifer and Baehner, Frederick L. and Fevr, Tea and Clark, Laura and Bayani, Nora and Coppe, Jean-Philippe and Tong, Frances }, citeulike-article-id = {989152}, doi = {10.1016/j.ccr.2006.10.008}, journal = {Cancer Cell}, keywords = {breast\_cancer}, month = {December}, number = {6}, pages = {515--527}, posted-at = {2007-09-30 06:38:33}, priority = {5}, title = {A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes}, url = {http://dx.doi.org/10.1016/j.ccr.2006.10.008}, volume = {10}, year = {2006} }

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TY - JOUR ID - citeulike:989152 L3 - citeulike-article-id:989152 TI - A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes JF - Cancer Cell VL - 10 IS - 6 SP - 515 EP - 527 N2 - SummaryRecent 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. KW - breast_cancer AU - Neve, Richard AU - Chin, Koei AU - Fridlyand, Jane AU - Yeh, Jennifer AU - Baehner, Frederick AU - Fevr, Tea AU - Clark, Laura AU - Bayani, Nora AU - Coppe, Jean-Philippe AU - Tong, Frances PY - 2006/12// UR - http://dx.doi.org/10.1016/j.ccr.2006.10.008 ER -

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