TY - JOUR
T1 - Dehydroepiandrosterone sulfate causes proliferation of estrogen receptor-positive breast cancer cells despite treatment with fulvestrant
AU - Calhoun, Kristine E.
AU - Pommier, Rodney F.
AU - Muller, Patrick
AU - Fletcher, William S.
AU - Toth-Fejel, Su Ellen
AU - Alberty, Roger E.
AU - Kebebew, Electron
AU - Goodnight, James E.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2003/8/1
Y1 - 2003/8/1
N2 - 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.
AB - 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.
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U2 - 10.1001/archsurg.138.8.879
DO - 10.1001/archsurg.138.8.879
M3 - Article
C2 - 12912747
AN - SCOPUS:0042532160
SN - 0004-0010
VL - 138
SP - 879
EP - 883
JO - Archives of Surgery
JF - Archives of Surgery
IS - 8
ER -