Dehydroepiandrosterone sulfate causes proliferation of estrogen receptor-positive breast cancer cells despite treatment with fulvestrant

Kristine E. Calhoun, Rodney F. Pommier, Patrick Muller, William S. Fletcher, SuEllen Toth-Fejel, Roger E. Alberty, Electron Kebebew, James E. Goodnight

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

Hypothesis: Dehydroepiandrosterone sulfate (DHEA-S) causes a proliferation of estrogen receptor (ER)-positive breast cancer cells, even with tamoxifen citrate blockade. The ER antagonist ICI 182 780 (fulvestrant) will more effectively stop the proliferative effect of DHEA-S on breast cancer cells. Design: Examination of in vitro breast cancer cell growth in the presence of fulvestrant and DHEA-S. Setting: Surgical oncology research laboratory. Interventions: The ER-positive and ER-negative breast cancer cells were pretreated with fulvestrant and stimulated with 900 pg/dL (22.8 pmol/L) of DHEA-S. Main Outcome Measures: Assays using 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide, thiazolyl blue, were performed on the third, fifth, and seventh days poststimulation and permitted the calculation of growth percent change. Results: The ER-positive and progesterone receptor-positive cells demonstrated universal proliferation of 107% by day 7 when treated with fulvestrant, regardless of the dose. The ER-negative and progesterone receptor-negative cells demonstrated growth inhibition. Conclusions: The DHEA-S circumvented fulvestrant inhibition and caused ER-positive breast cancer cell growth.

Original languageEnglish (US)
Pages (from-to)879-883
Number of pages5
JournalArchives of Surgery
Volume138
Issue number8
DOIs
StatePublished - Aug 1 2003

ASJC Scopus subject areas

  • Surgery

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