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Kristine E. Calhoun, MD; Rodney F. Pommier, MD; Patrick Muller, BS; William S. Fletcher, MD; SuEllen Toth-Fejel, PhD

Arch Surg. 2003;138:879-883.

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 µg/dL (22.8 µmol/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.

From the Division of Surgical Oncology, Department of General Surgery, Oregon Health and Sciences University, Portland.

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