We are analyzing https://link.springer.com/article/10.1007/s10549-008-0080-8.

Title:
The androgen metabolite 5α-androstane-3β,17β-diol (3βAdiol) induces breast cancer growth via estrogen receptor: implications for aromatase inhibitor resistance | Breast Cancer Research and Treatment
Description:
The aromatase inhibitors (AIs) are used to treat estrogen receptor-positive (ER+) breast tumors in post-menopausal women, and function by blocking the conversion of adrenal androgens to estrogens by the enzyme CYP19 aromatase. Breast cancer patients receiving AI therapy have circulating estrogen levels below the level of detection; however, androgen concentrations remain unchanged. We were interested in studying the effects of androgens on breast cancer cell proliferation under profound estrogen-deprived conditions. Using in vitro models of estrogen-dependent breast cancer cell growth we show that the androgens testosterone and 5α-dihydrotestosterone induce the growth of MCF-7, T47D and BT-474 cells in the absence of estrogen. Furthermore, we demonstrate that under profound estrogen-deprived conditions these breast cancer cells up-regulate steroidogenic enzymes that can metabolize androgens to estrogens. Lastly, we found that the downstream metabolite of 5α-dihydrotestosterone, 5α-androstane-3β,17β-diol (3βAdiol), is estrogenic in breast cancer cells, and induces growth and ER-signaling via activation of ERα. In conclusion, our results show that breast cancer cells deprived of estrogen up-regulate steroidogenic enzymes and metabolize androgens to estrogen-like steroids. The generation of estrogen-like steroids represents a potential mechanism of resistance to aromatase inhibitors.
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Keywords {🔍}

cancer, article, breast, pubmed, google, scholar, cas, estrogen, aromatase, growth, androgens, receptor, res, inhibitor, cells, rae, human, betadiol, prostate, usa, cell, research, androgen, metabolite, lippman, treat, steroids, medical, center, privacy, cookies, content, βadiol, james, access, steroid, beta, alphaandrostanebeta, data, publish, search, αandrostaneββdiol, resistance, study, sikora, cordero, larios, johnson, inhibitors, postmenopausal,

Topics {✒️}

month download article/chapter androgen derivative 5alpha-androstane-3beta long-term tissue culture androgen metabolite 5α-androstane-3β estrogen-dependent breast cancer treat estrogen receptor-positive profound estrogen-deprived conditions real-time quantitative pcr 4-hydroxy-n-desmethyl tamoxifen estrogen receptors alpha cyp7b1-mediated metabolism breast cancer cells aromatase-independent testosterone conversion full article pdf metastatic breast cancer advanced breast cancer aromatase inhibitor therapy privacy choices/manage cookies 5α-androstane-3β estrogen receptor beta estrogen receptor alpha 5 alpha-reductase inhibitor aromatase inhibitor resistance estrogen receptor expression 5α-dihydrotestosterone induce 5 alpha-androstane-3 beta 17β-diol ai 5alpha-androstane-3beta michigan medical center circulating estrogen levels transcript tissue distribution widespread tissue distribution enzyme cyp19 aromatase steroidal aromatase inactivators conditions privacy policy treatment article general medical sciences regulates prostate growth breast cancer european economic area regulate steroidogenic enzymes beneficial androgenic action related subjects gc/ms/ms ligand binding specificity cytochrome p450 aromatase post-menopausal women benign prostatic hyperplasia article sikora author information authors

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         description:The aromatase inhibitors (AIs) are used to treat estrogen receptor-positive (ER+) breast tumors in post-menopausal women, and function by blocking the conversion of adrenal androgens to estrogens by the enzyme CYP19 aromatase. Breast cancer patients receiving AI therapy have circulating estrogen levels below the level of detection; however, androgen concentrations remain unchanged. We were interested in studying the effects of androgens on breast cancer cell proliferation under profound estrogen-deprived conditions. Using in vitro models of estrogen-dependent breast cancer cell growth we show that the androgens testosterone and 5α-dihydrotestosterone induce the growth of MCF-7, T47D and BT-474 cells in the absence of estrogen. Furthermore, we demonstrate that under profound estrogen-deprived conditions these breast cancer cells up-regulate steroidogenic enzymes that can metabolize androgens to estrogens. Lastly, we found that the downstream metabolite of 5α-dihydrotestosterone, 5α-androstane-3β,17β-diol (3βAdiol), is estrogenic in breast cancer cells, and induces growth and ER-signaling via activation of ERα. In conclusion, our results show that breast cancer cells deprived of estrogen up-regulate steroidogenic enzymes and metabolize androgens to estrogen-like steroids. The generation of estrogen-like steroids represents a potential mechanism of resistance to aromatase inhibitors.
         datePublished:2008-06-04T00:00:00Z
         dateModified:2008-06-04T00:00:00Z
         pageStart:289
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      headline:The androgen metabolite 5α-androstane-3β,17β-diol (3βAdiol) induces breast cancer growth via estrogen receptor: implications for aromatase inhibitor resistance
      description:The aromatase inhibitors (AIs) are used to treat estrogen receptor-positive (ER+) breast tumors in post-menopausal women, and function by blocking the conversion of adrenal androgens to estrogens by the enzyme CYP19 aromatase. Breast cancer patients receiving AI therapy have circulating estrogen levels below the level of detection; however, androgen concentrations remain unchanged. We were interested in studying the effects of androgens on breast cancer cell proliferation under profound estrogen-deprived conditions. Using in vitro models of estrogen-dependent breast cancer cell growth we show that the androgens testosterone and 5α-dihydrotestosterone induce the growth of MCF-7, T47D and BT-474 cells in the absence of estrogen. Furthermore, we demonstrate that under profound estrogen-deprived conditions these breast cancer cells up-regulate steroidogenic enzymes that can metabolize androgens to estrogens. Lastly, we found that the downstream metabolite of 5α-dihydrotestosterone, 5α-androstane-3β,17β-diol (3βAdiol), is estrogenic in breast cancer cells, and induces growth and ER-signaling via activation of ERα. In conclusion, our results show that breast cancer cells deprived of estrogen up-regulate steroidogenic enzymes and metabolize androgens to estrogen-like steroids. The generation of estrogen-like steroids represents a potential mechanism of resistance to aromatase inhibitors.
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      dateModified:2008-06-04T00:00:00Z
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         Estrogen receptor
         Oncology
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