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Prostate cancer cell lines lack amplification: overexpression of HER2.

Abstract
The potential overexpression of HER2 in prostate cancer cells has attended significant interest during the past few years, both as potential target for HER2 pathway focused therapy and as a mechanism involved in the progression to androgen independence. Conflicting results have been reported concerning HER2 status on clinical material, differences which generally have been attributed to methodological differences. Nevertheless, HER2 has been utilized for targeted therapy of prostate cancer in a number of preclinical studies and is still regarded as an exciting target molecule. In this study, the HER2 status of three widely used prostate cancer cell lines and corresponding xenografts has been analysed. By use of validated and FDA approved analytical staining techniques none of these cell lines or xenografts were shown to overexpress/amplify HER2, as demonstrated by immunohistochemistry and fluorescence in situ hybridization. These findings are important for the interpretation and understanding of the therapeutic effects when developing drugs targeting HER2 in prostate cancer cell lines and also emphasize the importance of using broad and validated analytical techniques.
AuthorsAnders Ullén, Lena Lennartsson, Ulrika Harmenberg, Bo Lennernäs, Khairul Majumder, Anders R Holmberg, Sten Nilsson, Göran P Elmberger
JournalActa oncologica (Stockholm, Sweden) (Acta Oncol) Vol. 44 Issue 5 Pg. 490-5 ( 2005) ISSN: 0284-186X [Print] England
PMID16118083 (Publication Type: Evaluation Study, Journal Article)
Chemical References
  • Antibodies, Monoclonal
  • Biomarkers, Tumor
  • Receptor, ErbB-2
Topics
  • Animals
  • Antibodies, Monoclonal
  • Biomarkers, Tumor (metabolism)
  • Breast Neoplasms, Male (genetics, metabolism)
  • Cell Line, Tumor
  • Gene Expression Regulation, Neoplastic
  • Genes, erbB-2
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization, Fluorescence
  • Male
  • Mice
  • Prostatic Neoplasms (metabolism)
  • Receptor, ErbB-2 (biosynthesis)
  • Up-Regulation

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