Actions of a progestin derived from 19-norprogestérone on the mammary gland: The nomégestrol acetate

Type :

Term papers

Pages :

14 pages

Format :

.doc

Published date :

06/21/2009

Category :

Science & technology

Sub category :

Medical studies

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Summary :

Introduction
Regulation of progesterone receptor
Nomegestrol biological effects of acetate on the breast
Nomegestrol effects of acetate on the enzyme activities involved in the biosynthesis of E2
Intramammary
Nomegestrol effects of acetate on cell proliferation and apoptosis in breast Mammary apoptosis
Nomegestrol effects of acetate on the drug resistance of breast cancer cells
Tolerance breast clinic
Radiological breast density
Conclusion
References

Abstract

Réceptologie work showed that the acetate nomégestrol a high specificity and affinity for the progesterone receptor, especially in the normal human breast tissue and cancer. It significantly inhibits the synthesis of progesterone receptors in breast cancer cells, hormone-dependent human T-47D in a culture in estrogen, which reflects its strong activity progestogen. However, it has no affinity for the estrogen receptor and is devoid of any estrogenic potential, as confirmed by the absence of induction of alkaline phosphatase activity in Ishikawa cells. The nomégestrol acetate inhibits the synthesis of estrogen receptors in estrogen-induced, mechanism of action of its anti-estrogenic activity intrinsic marked. Finally, it is devoid of any androgenic activity, in contrast to androgenic progestins (derived from 19-nortestosterone, medroxyprogesterone acetate) may have an indirect impact on the breast by the changes in the synthesis of SHBG (sex hormone binding globulin) and the IGF-I (insulin-like growth factor-I) induced. In work on the effects of progestogens on the enzyme activities involved in the biosynthesis of intramammary estradiol (E2), the nomégestrol acetate in vitro is able to control the levels of E2 in cancerous breast tissue: it blocks the formation of 'E2 in human breast cancer cells MCF-7 and T-47D by inhibiting the activity of the sulfatase that allows the conversion of estrone sulfate (E1S) into estrone (E1) and the 17β-hydroxysteroid dehydrogenase type 1, which catalyzes the conversion of E1 into E2. In addition, it stimulates the activity of the sulfotransferase and therefore the transformation of non-conjugated estrogens E1 and E2 in estrogen sulfates, biologically inactive. Work in vitro on cell proliferation have highlighted the one hand, the absence of stimulation by acetate nomégestrol the proliferation of MCF-7 cells cultured in a medium devoid of estrogens and on the other hand, a nomégestrol antiproliferative effect of acetate on T-47D cells in estrogen.