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

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

    Research output: Contribution to journalArticle

    16 Citations (Scopus)

    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

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    Dehydroepiandrosterone Sulfate
    Estrogen Receptors
    Breast Neoplasms
    Dehydroepiandrosterone
    Progesterone Receptors
    Growth
    Tamoxifen
    fulvestrant
    Outcome Assessment (Health Care)
    Research

    ASJC Scopus subject areas

    • Surgery

    Cite this

    Dehydroepiandrosterone sulfate causes proliferation of estrogen receptor-positive breast cancer cells despite treatment with fulvestrant. / Calhoun, Kristine E.; Pommier, Rodney; Muller, Patrick; Fletcher, William S.; Toth-Fejel, SuEllen; Alberty, Roger E.; Kebebew, Electron; Goodnight, James E.

    In: Archives of Surgery, Vol. 138, No. 8, 01.08.2003, p. 879-883.

    Research output: Contribution to journalArticle

    Calhoun, Kristine E. ; Pommier, Rodney ; Muller, Patrick ; Fletcher, William S. ; Toth-Fejel, SuEllen ; Alberty, Roger E. ; Kebebew, Electron ; Goodnight, James E. / Dehydroepiandrosterone sulfate causes proliferation of estrogen receptor-positive breast cancer cells despite treatment with fulvestrant. In: Archives of Surgery. 2003 ; Vol. 138, No. 8. pp. 879-883.
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    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.",
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    AU - Fletcher, William S.

    AU - Toth-Fejel, SuEllen

    AU - Alberty, Roger E.

    AU - Kebebew, Electron

    AU - Goodnight, James E.

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