| pubmed-article:6850519 | pubmed:abstractText | Hormones have been shown experimentally to act as cocarcinogens or promoters, i.e., they facilitate the carcinogenic event. In the cases of breast and endometrium, those hormones that facilitate growth may also favor carcinogenesis in the human. There is good epidemiologic evidence that use of estrogens after the menopause increases the incidence of breast and endometrial cancer, the risk increasing with increasing duration of use. Periodic progestin-induced withdrawal will probably mitigate the risk of endometrial cancer after the menopause. Prolactin is the important promoter of mammary cancer in the rat and mouse, but its significance in women is still under study. Intermittently elevated prolactin levels have been noted in some women who subsequently developed breast cancer, but epidemiologic studies of women who have received prolactin-releasing drugs such as reserpine and perphenazine have not disclosed increased risk. Diethylstilbestrol is listed as a carcinogen but any estrogen can induce mammary cancer in the rodent or vaginal adenosis in the neonatal mouse (an experimental model of human vaginal adenocarcinoma). | lld:pubmed |
