Understanding the biologic mechanisms responsible for breast-cancer progression during tamoxifen or fulvestrant treatment

Chelsea Hardin, Rodney Pommier, Brett Lefleur, Terisa Jackson, Su Ellen Toth-Fejel

    Research output: Contribution to journalArticle

    1 Scopus citations

    Abstract

    Dehydroepiandosterone sulfate (DHEAS) causes breast-cancer proliferation, even during tamoxifen or fulvestrant blockade. The purpose of this study was to determine possible mechanisms for this treatment failure. T-47D cells (estrogen receptor [ER] and progesterone receptor [PR] positive) were treated with fulvestrant (10 mol/L), tamoxifen (10 mmol/L or 0.0001 nmol/L), or vehicle and stimulated with DHEAS. Gene expression of ER, PR, insulin-like growth factor (IGF)-1 and -2, and insulin-like growth-factor binding protein (IGFBP)-1 through -4 was determined. ER and PR gene expression decreased by 1.3- and 4-fold with fulvestrant and DHEAS. ER expression decreased by 2.7-fold with 0.0001 nmol/L tamoxifen and DHEAS. ER and PR expression were unchanged by 10 nmol/L tamoxifen. IGF-1 and IGF-2 were not expressed. IGFBP-2 and -4 expression decreased by 1.9- and 1.6-fold after DHEAS stimulus, although this was not statistically significant. DHEAS exposure, even in the presence of tamoxifen and fulvestrant, induces changes in ER and PR gene expression that may be partially responsible for breast cancer progression.

    Original languageEnglish (US)
    Pages (from-to)426-428
    Number of pages3
    JournalAmerican journal of surgery
    Volume188
    Issue number4 SPEC. ISS.
    DOIs
    StatePublished - Oct 2004

    Keywords

    • Breast cancer
    • Dehydroepiandosterone sulfate
    • Estrogen receptor
    • Fulvestrant
    • Insulin-like growth factor
    • Tamoxifen

    ASJC Scopus subject areas

    • Surgery

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