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- W1990698400 abstract "The actions of estrogen (E) and progestogen (P) on normal endometrium are reviewed in order to give insight into endometrial hyperplasia and carcinoma. The entry of E from plasma may be protein-mediated. Human endometrium slices metabolize estradiol-17beta to an extent which varies with the stage of the cycle. Endometrium with cystic or anovulatory hyperplasia or adenocarcinoma behaves as proliferative endometrium. P in rats blocked E-induced replenishment of cytoplasmic receptors and caused a decrease in the quantity of cytoplasmic E receptors. Estrone and estriol had less affinity in binding to receptors than estradiol-17beta and this is important as a factor in the biological effect of these steroids. It has been noticed that the length of time the estrogen-receptor complex remains in the nucleus is a factor of critical importance for the biological potency as well. Weak estrogens may be as effective as estradiol-17beta if administered often enough. P enters the target cells through simple diffusion. Estradiol-17beta induces synthesis of new P uterine receptors while P itself seems to inactivate its own receptor. The role of E in the development of endometrial cancer is discussed. Results from a Swedish study suggest that prolonged estrogen stimulation unopposed by P can produce endometrial hyperplasia with a progression of changes leading to endometrial carcinoma. It is suggested that until the role of E in endometrial carcinoma is elucidated E should be administered only for established indications and only in a cyclical manner." @default.
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- W1990698400 date "1977-01-01" @default.
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- W1990698400 title "Endometrial Hyperplasia and Carcinoma: Histopathology and Hormonal Factors" @default.
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- W1990698400 doi "https://doi.org/10.3109/00016347709156346" @default.
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