Ovarian estrogen, inhibitor

In premenopausal women the ovary is the richest source of aromatase and hence estrogen. Aromatase is confined to the granulosa cells and is produced under the influence of gonadotropins (FSH and LH). Despite being a rich source of aromatase, three separate studies have shown that aromatase inhibitors are unable to sufficiently suppress ovarian estrogen production to postmenopausal levels. One explanation for this phenomenon may be a compensatory rise in gonadotrophins which maintains adequate estrogen production, despite the presence of the inhibitor. As such aromatase inhibitors cannot be used in premenopausal breast cancer patients. After menopause, ovarian... 

THE OVARY (ESTROGENS, PROGESTINS, OTHER OVARIAN HORMONES, ORAL CONTRACEPTIVES, INHIBITORS ANTAGONISTS, OVULATION-INDUCING AGENTS)... 

The Ovary (Estrogens, Progestins, Other Ovarian Hormones, Oral Contraceptives, Inhibitors Antagonists, Ovulation-Inducing Agents)... 

Aromatase inhibitors serve to eliminate ex-traovarian synthesis of estrogens in breast cancer patients. This can be achieved effectively only in postmenopause because, as an FSH-dependent enzyme, ovarian aromatase is subject to feedback regulation of female Luellmann, Color Atlas of Pharmacology 2005 Thieme All rights reserved. Usage subject to terms and conditions of license. 

While the inhibition of aromatase activity by PED is well established, some controversy exists as to its inhibition of tumor growth in vivo. Zimniski and coworkers and Puett and coworkers showed that PED was a potent inhibitor of dimethylbenzanthracene-induced mammary tumor growth at a dose of 1 mg/kg/day as well as of human ovarian carcinoma in athymic mice. In contrast, di Salle and coworkers and Zaccheo and coworkers " found that PED did not affect the growth of established tumors in the same model, nor did it prevent the appearance of new neoplasms. Thus, it appears that more in vivo studies on the inhibition of tumor growth are required before firm conclusions can be drawn on its role in estrogen-dependent tumor biology. 

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