HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Free Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Kauraniemi, P Articles by Kallioniemi, A Search for Related Content PubMed PubMed Citation Articles by Kauraniemi, P Articles by Kallioniemi, A

Laboratory of Cancer Biology and
¹ Laboratory of Cancer Genetics, University of Tampere and Tampere University Hospital, 33014 Tampere, Finland

(Requests for offprints should be addressed to P Kauraniemi; Email: paivikki.kauraniemi{at}uta.fi)

During the past decade the role of the ERBB2 (neu/HER2) oncogene as an important predictor of patient outcome and response to various therapies in breast cancer has been clearly established. This association of ERBB2 aberrations with more aggressive disease and poor clinical outcome, together with the high prevalence of such alterations in breast cancer, has also made ERBB2 an attractive target for therapy. A specific antibody-based therapy, Herceptin, directed against the extracellular domain of the ERBB2 receptor tyrosine kinase, was recently developed and several clinical trials have shown the therapeutic efficacy of this drug against ERBB2-positive breast cancer. However, a relatively large fraction of patients does not benefit from Herceptin treatment, indicating that other factors beyond ERBB2 itself must influence therapy response in ERBB2-positive tumors. It is well known that amplification of the 17q12–q21 region is the most common mechanism for ERBB2 activation in breast cancer and that it leads to simultaneous activation of several other genes. These co-amplified and co-activated genes may have an impact on disease progression and the clinical behavior of ERBB2-positive tumors and thus represent important targets of research. In this paper we discuss the current knowledge on the structure of the ERBB2 amplicon, the genes involved, and their possible contribution to breast cancer pathogenesis.

This article has been cited by other articles:

				A. Vincent-Salomon, C. Lucchesi, N. Gruel, V. Raynal, G. Pierron, R. Goudefroye, F. Reyal, F. Radvanyi, R. Salmon, J.-P. Thiery, et al. Integrated Genomic and Transcriptomic Analysis of Ductal Carcinoma In situ of the Breast Clin. Cancer Res., April 1, 2008; 14(7): 1956 - 1965. [Abstract] [Full Text] [PDF]

				T. Bai and S.-W. Luoh GRB-7 facilitates HER-2/Neu-mediated signal transduction and tumor formation Carcinogenesis, March 1, 2008; 29(3): 473 - 479. [Abstract] [Full Text] [PDF]

				A. Belkhiri, A. A. Dar, A. Zaika, M. Kelley, and W. El-Rifai t-Darpp Promotes Cancer Cell Survival by Up-regulation of Bcl2 through Akt-Dependent Mechanism Cancer Res., January 15, 2008; 68(2): 395 - 403. [Abstract] [Full Text] [PDF]

				G. Alexe, G. S. Dalgin, D. Scanfeld, P. Tamayo, J. P. Mesirov, C. DeLisi, L. Harris, N. Barnard, M. Martel, A. J. Levine, et al. High Expression of Lymphocyte-Associated Genes in Node-Negative HER2+ Breast Cancers Correlates with Lower Recurrence Rates Cancer Res., November 15, 2007; 67(22): 10669 - 10676. [Abstract] [Full Text] [PDF]