Original Paper

Oestrogen receptor gene (ESR1) amplification is frequent in endometrial carcinoma and its precursor lesions†

  1. A Lebeau1,‡,
  2. TJ Grob1,‡,
  3. F Holst1,
  4. N Seyedi-Fazlollahi1,
  5. H Moch2,
  6. Luigi Terracciano3,
  7. A Turzynski4,
  8. M Choschzick1,
  9. G Sauter1,
  10. R Simon1,*

Article first published online: 14 JUL 2008

DOI: 10.1002/path.2405

Issue

The Journal of Pathology

The Journal of Pathology

Volume 216, Issue 2, pages 151–157, October 2008

Additional Information

How to Cite

Lebeau, A., Grob, T., Holst, F., Seyedi-Fazlollahi, N., Moch, H., Terracciano, L., Turzynski, A., Choschzick, M., Sauter, G. and Simon, R. (2008), Oestrogen receptor gene (ESR1) amplification is frequent in endometrial carcinoma and its precursor lesions. J. Pathol., 216: 151–157. doi: 10.1002/path.2405

Author Information

  1. 1

    Institute of Pathology, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany

  2. 2

    Institute of Pathology, University of Zurich, Switzerland

  3. 3

    Institute of Pathology, University of Basel, Switzerland

  4. 4

    Consultant in Pathology, Pferdemarkt 12, Lübeck, Germany

  1. ‡

    These two authors contributed equally to this study.

*Institute of Pathology, University Medical Centre Hamburg-Eppendorf, Martinistrasse 25, 20246 Hamburg, Germany.

  1. †

    Conflict of interest: the University Medical Centre Hamburg-Eppendorf has filed a patent application for certain technology described in this paper.

  2. ‡

    These two authors contributed equally to this study.

Publication History

  1. Issue published online: 2 SEP 2008
  2. Article first published online: 14 JUL 2008
  3. Accepted manuscript online: 14 JUL 2008 12:00AM EST
  4. Manuscript Accepted: 26 JUN 2008
  5. Manuscript Revised: 18 JUN 2008
  6. Manuscript Received: 15 JAN 2008

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Keywords:

  • oestrogen receptor;
  • ESR1;
  • endometrial carcinoma;
  • tamoxifen;
  • amplification

Abstract

Oestrogen receptor alpha (ER) plays a critical, diverse and not fully understood role in endometrial carcinoma. Most endometrial carcinomas express ER and some of these tumours respond favourably to anti-oestrogen therapy. On the other hand, tamoxifen therapy constitutes a major risk factor for endometrial carcinoma development. Amplification of the ESR1 gene encoding ER was recently shown to constitute a mechanism for ER over-expression in breast carcinoma. This study was designed to determine the potential role of ESR1 amplifications in endometrial carcinoma. Tissue microarrays of 368 endometrial carcinomas and large sections of 43 cases of endometrial hyperplasia were analysed for ESR1 gene amplification and ER protein expression by means of fluorescence in situ hybridization (FISH) and immunohistochemistry. FISH revealed ESR1 amplification in 40/176 (23%) cancers, 6/19 (32%) atypical complex hyperplasias, 3/10 (30%) complex hyperplasias without atypia and 2/14 (14%) simple hyperplasias without atypia. Strong ER protein expression was significantly linked to ESR1 amplification in endometrial carcinoma (p = 0.0036). These data indicate that ESR1 amplification might be one mechanism for ER over-expression in endometrial carcinoma, and suggest an early role for ESR1 amplification in the development of a significant fraction of endometrial carcinoma. Given the predictive role of ESR1 amplification for tamoxifen response in breast carcinoma, it will be interesting to investigate the response of ESR1-amplified endometrial cancers to anti-oestrogenic drugs. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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