An association between endometrial hyperplasia and corpus cancer has long been suspected. Genetically predisposed women are at greater risk of developing endometrial cancer if subjected to long uninterrupted period of estrogen stimulation. Endometrial cancer need not be inevitable if 14 day courses of an oral progestogen are continued for as long as is necessary; in some women, however, the lesions will progress and, therefore, should be carefully followed with repeated endometrial biopsies. Epidemiological evidence suggests a true link between unopposed estrogens and early, less invasive endometrial cancer, and progestogens appear capable of protecting against the development of cancer and hyperplasia, although complete protection has not yet been achieved. The protective action of progestogens is supported by the fact the none developed endometrial cancer in a series of 490 women of reproductive age who received continuous estrogens by way of pellet implants of 17 beta estradiol for conception control for 1--10 years. Evidence for the protective action of progestogens in estrogen-treated menopausal women was less solid than in non-menopausal women but was nonetheless considerable. Our study of 1058 women, 45 years of age and older, receiving continuous estrogens by way of 17 beta estradiol pellets over a period varying from 1 to 21 years, revealed that the incidence of cancer was not greater and was possibly less than that expected in an untreated population of menopausal women.

作者：R B, Greenblatt；R D, Gambrell；L D, Stoddard

来源：Pathology, research and practice 1982 年 174卷 3期