Pommier RF, Woltering EA, Keenan EJ, Fletcher WS.
Department of Surgery, Oregon Health Sciences University, Portland 97201.
Fifteen patients whose tumors progressed while they received tamoxifen citrate therapy were studied by serial determinations of serum levels of estrone (E1), estradiol (E2), and dehydroepiandrosterone (DHEA) obtained during progression after withdrawal from tamoxifen therapy and total endocrine ablation or suppression. Discontinuation of tamoxifen therapy resulted in reductions of DHEA, E1, and E2 levels by 44%, 49%, and 42%, respectively. Ablation or suppression reduced sex steroids to minimal levels and produced responses in all patients. Elevations of DHEA, E1, and E2 could be provoked by readministering tamoxifen to hypophysectomized and oophorectomized, but not adrenalectomized, patients, indicating that the adrenal gland is the source of these sex steroids. We conclude that tamoxifen stimulates adrenal production of DHEA, which is aromatized to E1 and E2. Buildup of E1 and E2 overwhelms the competitive binding of tamoxifen to the estrogen receptor, resulting in tumor progression.
Jak pisalem blokuje receptor a sam w sobie moze nawet podwyzszac estro (tu jako powod podaja aromatyzacje dhea podwyzszonego przez tamox)
Niestety nawet na sile nie zmienisz dzialania tamoxu heheeh
".... Then we'll see which are better, his steroids or mine"