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

by: R.M. Neve, K. Chin, J. Fridlyand, J. Yeh, F.L. Baehner, T. Fevr, L. Clark, N. Bayani, J.P. Coppe, F. Tong, T. Speed, P.T. Spellman, S. DeVries, A. Lapuk, N.J. Wang, W.L. Kuo, J.L. Stilwell, D. Pinkel, D.G. Albertson, F.M. Waldman, F. McCormick, R.B. Dickson, M.D. Johnson, M. Lippman, S. Ethier, A. Gazdar, and J.W. Gray

In: Cancer Cell, Vol. 10, Nr. 6 (2006) , p. 515--527.

Abstract

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.

BibTeX record

@article{260,
  abstract = {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.},
  added-at = {2008-10-17T17:04:38.000+0200},
  author = {Neve, R.M. and Chin, K. and Fridlyand, J. and Yeh, J. and Baehner, F.L. and Fevr, T. and Clark, L. and Bayani, N. and Coppe, J.P. and Tong, F. and Speed, T. and Spellman, P.T. and DeVries, S. and Lapuk, A. and Wang, N.J. and Kuo, W.L. and Stilwell, J.L. and Pinkel, D. and Albertson, D.G. and Waldman, F.M. and McCormick, F. and Dickson, R.B. and Johnson, M.D. and Lippman, M. and Ethier, S. and Gazdar, A. and Gray, J.W.},
  biburl = {http://www.bibsonomy.org/bibtex/2e01881e32ea27d97d05fff62470c0810/biobibs_matthew},
  id = {info:sici/1535-6108(2006)10<515:ACOBCC>2.0.CO;2-0,
             info:doi/10.1016/j.ccr.2006.10.008, info:pmid/17157791},
  interhash = {346351f5c69b335d0e53b9ea746fa962},
  intrahash = {e01881e32ea27d97d05fff62470c0810},
  issn = {1535-6108},
  journal = {Cancer Cell},
  keywords = {imported},
  number = 6,
  pages = {515--527},
  timestamp = {2008-10-17T17:04:38.000+0200},
  title = {A collection of breast cancer cell lines for the study of
             functionally distinct cancer subtypes},
  volume = 10,
  year = 2006
}

Endnote record

%0 Journal Article
%1 260
%A Neve, R.M.
%A Chin, K.
%A Fridlyand, J.
%A Yeh, J.
%A Baehner, F.L.
%A Fevr, T.
%A Clark, L.
%A Bayani, N.
%A Coppe, J.P.
%A Tong, F.
%A Speed, T.
%A Spellman, P.T.
%A DeVries, S.
%A Lapuk, A.
%A Wang, N.J.
%A Kuo, W.L.
%A Stilwell, J.L.
%A Pinkel, D.
%A Albertson, D.G.
%A Waldman, F.M.
%A McCormick, F.
%A Dickson, R.B.
%A Johnson, M.D.
%A Lippman, M.
%A Ethier, S.
%A Gazdar, A.
%A Gray, J.W.
%D 2006
%J Cancer Cell
%K 
%N 6
%P 515--527
%T A collection of breast cancer cell lines for the study of
             functionally distinct cancer subtypes
%V 10
%X 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.