gms | German Medical Science

27. Deutscher Krebskongress

Deutsche Krebsgesellschaft e. V.

22. - 26.03.2006, Berlin

Exposure of breast cancer cells to electromagnetic fields differentially alters gene expression of estrogen receptor cofactors

Meeting Abstract

Suche in Medline nach

  • corresponding author presenting/speaker Rainer Girgert - Universitätsfrauenklinik, Göttingen, Deutschland
  • Carsten Grünker - Universitätsfrauenklinik, Göttingen
  • Günter Emons - Universitätsfrauenklinik, Göttingen
  • Volker Hanf - Frauenklinik, Fürth

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocPO015

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dkk2006/06dkk125.shtml

Veröffentlicht: 20. März 2006

© 2006 Girgert et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Environmental factors like estrogenic chemicals and electromagnetic fields are suspected to contribute to the increased incidence of breast cancer in industrialized countries. The mechanism by which electromagnetic fields influence the growth of breast cancer cells is not fully characterized. Decreased melatonin levels in serum has been discussed as one possible cause. The efficacy of the antiestrogenic drug tamoxifen is also decreased by electromagnetic fields. The mechanism leading to this reproducible effect was the subject of this study.

MCF-7 breast cancer cells from two different sources were exposed for various time intervals to 50 Hz electromagnetic fields in specially designed incubators. Proliferation of the breast cancer cells in the presence of tamoxifen was measured in a shielded configuration (0µT) and at 1.2 µT, 10 µT and 100 µT resp. The expression of estrogen receptor cofactors was determined by RT-PCR using RNA from cells exposed to 1.2 µT for 24 or 48 hours.

Electromagnetic fields shifted the dose-response curve of tamoxifen to higher concentrations. This effect was higher at 1.2 µT than at 10 µT or 100µT. In addition, one tested clone of MCF-7 cells even showed an increased proliferative response at 10-7M tamoxifen, if 1.2 µT were applied. ER coactivators: exposure to 1.2 µT increased the expression of AIB-1 (amplified in breast cancer) in both MCF-7 clones after 24 hours, SRC-1 expression was only increased in one clone after 48 hours. The corepressor N-CoR decreased in one clone after 24 hours and in the other clone only after 48 hours. SMRT decreased in both after 48 hours.

Electromagnetic fields induce a behavior of the breast cancer cells similar to the frequently observed tamoxifen resistance in the clinical setting. 1) The shift of the dose-response curve of tamoxifen to higher concentrations in the magnetic field leads to a reduced efficacy of tamoxifen at therapeutic concentrations. 2) At 10-7M, a concentration achieved in the serum of patients treated with tamoxifen, proliferation of the breast cancer cells is even enhanced. 3) In tamoxifen resistant tumors expression of coactivators is increased and corepressors are decreased.