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Query: UMLS:C0476089 (endometrial cancer)
11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concensus conclusions reached at a concensus development conference on Estrogen Use and Postmenopausal Women in September 1979 are based on 3 position papers prepared for the conference, the response of the panel, and the general discussion by the audience, followed by the panel and other conference participants. The evidence for the efficacy of estrogens in treating specific conditions associated with menopause was reviewed 1st. It was accepted that estrogens are more effective than placebo in decreasing the frequency and severity of vasomotor symptoms. Estrogens are effective in overcoming the atrophy of the vaginal epithelium and the associated symptoms. Present evidence does not justify the use of estrogens to treat primary psychological problems. The validity of 3 randomized trials indicating that exogenous estrogens can retard bone loss if given around the time of menopause was acknowledged. There is no convincing evidence that estrogens in customary doses increase the risk of thromboembolic phenomena, stroke, or heart disease in women who have undergone natural menopause. Evidence was also reviewed concerning adverse effects associated with post-menopausal estrogen use. In the absence of exogenous estrogens, the incidence of endometrial cancer is about 1/1000 postmenopausal women per year. This rate increases severalfold beginning after about 2-4 years of use of 0.625 or 1.25 mg of conjugated estrogens daily. Cystic hyperplasia of the endometrium, regarded as a premalignant condition, has been associated with unopposed estrogen, whether endogenous or exogenous.
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PMID:Estrogen use and postmenopausal women: a National Institutes of Health Consensus Development Conference. 4 37

The effects of long-term estrogen replacement therapy upon neoplastic diseases were studied in 301 treated patients and 309 untreated patients. 207 women of each group had uteri in situ. Incidence figures for neoplasia were compared between the 2 groups and with the Third National Cancer Survey, yielding a risk ratio for the development of adenocarcinoma of the endometrium among estrogen-treated women of 3.8 (p .05) and 9.3, respectively. The addition of synthetic progestin to estrogen therapy provided significant (p .001) protection against the likelihood of developing endometrial cancer and did not reduce previously reported metabolic benefits of estrogen treatment. The data did not show an increased incidence of breast cancer among estrogen treated women, even with higher dosages or long-term therapy. It is recommended that estrogen therapy should be instituted whenever appropriate indications are present and no major contraindications exist; estrogen should be administered in the lowest dosage and duration that can adequately treat the indication for its use. Estrogens should probably be administered in cyclic fashion, especially if the uterus is in place, with sequentially added progestin.
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PMID:Effects of long-term estrogen replacement therapy. II. Neoplasia. 22 Aug 75

An overview of the sex hormones is presented. Testosterone is a natural androgen produced in the testes, adrenal glands, and ovaries. It has anabolic as well as androgenic effects. Testosterone is used to treat inoperable breast cancer and osteoporosis, and to stimulate erythropoesis. Androgens are absolutely counterindicated in cases of prostate cancer. Estrone, estradiol, and estriol are natural estrogens produced in the ovaries, placenta, testes, and adrenal glands. These hormones also influence the production of gonadotropins by the pituitary gland. Estrogens are used to treat menopausal disorders, ovarial insufficiency, estrogen-independent breast cancer, prostate cancer, and in some cases pregnancy disorders. Estrogens and progestagens are 2 components used in oral contraceptives. Progesterone, a natural progestagen, is produced by the corpus luteum. It promotes the proliferation phase of the endometrium, fertilization, and nidation, and it works to maintain pregnancy. Progesterone is used to treat spontaneous abortion, corpus luteum insufficiency, and endometrial cancer.
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PMID:[Sex hormones]. 24 26

Estrogens and progesterone seem to have at times antagonistic, at times synergetic action on breast and uterine tissues. While estrogens stimulate cell proliferation, progestrerone favors secretion. While estrogens favor myometrial and endometrial hyperplasia, progesterone seems to dominish congestive phenomena caused by estrogens, especially on breast tissues. Women who experience menopause at 55 have a twice as high risk of breast cancer than women who menopause at 45. Breast and endometrial cancer are often associated with a history of menstrual disorders, and it is very possible that endometrial hyperplasia and cystic mastosis are connected. While treatment with estrogens helps to avoid vaginal atrophy and to arrest osteoporosis, it is doubtful whether the treatment should be systematic over 45. Breast examination and a thorough gynecological examination are essential once a year.
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PMID:[Menopause, estrogens and genital cancer]. 24 20

Estrogens do not have the general biological effect of increasing the occurrence of cancer in various species of laboratory animals. The neoplastic effect of estrogens in animals is strain and species dependent. Estrogens may increase the incidence of uterine cervical cancer in some strains of mice, but not in other strains or other animal species. The progestins and oral contraceptives (OC) have not induced cervical cancer in animals and most studies demonstrate that the steroid anovulants do not increase the occurrence of abnormal cervical smears or cervical cancer in women. Estrogens increase the occurrence of endometrial cancer in the rabbit, occasionally in the mouse, but apparently not in other species. Case-control studies in menopausal and postmenopausal women indicate an increased risk of endometrial carcinoma (EC) associated with use of estrogen. However, in other studies estrogen has not been related to EC. Cases of EC have been reported in women using sequential OC but a causal relationship has not been established. Progestins alone may arrest progress or cause regression of EC in women. EC has not been related to use of the combination OC, and it is unlikely that use of these anovulants will lead to the development of endometrial cancer. Estrogens or OC do not induce a carcinogenic response in the ovary. A decrease in ovarian cysts, is observed during the clinical use of OC.
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PMID:Evaluation of the carcinogenic effects of estrogens, progestins and oral contraceptives on cervix, uterus and ovary of animals and man. 28 71

Hormones may act as promoters in the carcinogenic process, and occasionally their metabolites may act as antihormones or have new physiologic effects. Drugs can interact with the endocrine system in many ways. They can promote secretion of a hormone, alter its rate of removal from plasma, change plasma protein-binding characteristics, or modify routes of metabolism. Estrogens have a preparative effect on the uterine endometrium. There are biologic, clinical and epidemiologic reasons for believing that estrogen administration to postmenopausal women increases the risk for endometrial cancer. Although there are similar biologic reasons to associate prolonged estrogenic stimulation with breast cancerr, evidence for such an association is weak. Oral contraceptive use has been associated with a variety of hepatocellular tumors. Although estrogens, per se, can effect several hepatic functions, it seems likely that the 17 alpha-alkyl and 17 alpha-ethinyl functions of the progestins and estrogens are involved in this process. The role of estrogen use during pregnancy in the causation of vaginal cancer in female offspring and the role of androgens in prostate cancer have been discussed.
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PMID:Interaction of drugs, hormones, and nutrition in the causes of cancer. 37 2

This lengthy discussion of possible associations between both endogenous and exogenous estrogens and progestins to occurrence of human cancers begins by discussing endogenous metabolism of the 2 sex steroid types. For example, the endogenous production of estrogen is associated with anovulation and endometrial cancer, although clearly other risk factors are associated with these diseases, and breast cancer, which account for some or all of the sex hormones apparent carcinogenic effect. Also discussed are the modulating effects of estriol on response of the breast and endometrium to estradiol and estrogens, and the modulating effects of androgens on development of breast cancer. The bulk of the monograph concerns summaries of data on the correlations of exogenous sex hormones and human cancers. Attention is also paid to the use of exogenous sex hormones for treatments of human cancers. Estrogens have been used to treat endometrial cancer, breast cancer, and benign breast disease. Side effects of hormonal contraception discussed include gross and microscopic changes in the breast, benign breast disease, and breast cancer; in the uterus, exogenous hormonal contraception is associated with neoplastic changes in the cervix, cervical neoplasia, endometrial cancer, trophoblastic tumors, and uterine fibroids. Ovarian effects include nonneoplastic and benign lesions and ovarian cancers. Oral contraception may also correlate with incidences of pituitary and melanoma malignancies. Liver effects include both benign neoplasms and malignant tumors.
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PMID:Oestrogens and progestins in relation to human cancer. 39 83

3 studies reviewed by the Federal Drug Administration (FDA) have concluded that new research affirms that menopausal and postmenopausal women who take estrogens have an increased risk of endometrial cancer. The data also supports estrogen labelling which advises health professionals and women patients that the risk is reduced if estrogens are taken in the lowest possible dose and if chronic administration is avoided. Increased risk of endometrial cancer in estrogen users is proportional to the duration of use and is particularly high with use over 5 years. Increased risk was reported for use of 1-5 years. Cyclic therapy or progestins for 7 days each month does not protect against the risk of endometrial cancer. Use of progestins for longer periods has not been proven to provide adequate protection and not been adequately studied. Women who have uterine bleeding after estrogen therapy receive increased diagnostic attention, and their cancer is detected earlier than women not taking the drugs. Although women with endometrial cancer who take estrogens may be diagnosed sooner, ultimately all women with endometrial cancer will be diagnosed. Estrogens are effective for vasomotor symptoms of the menopause and can be used with no known increase in risk for treatment if doses are kept low and duration is less than 1 year.
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PMID:Update on estrogens and uterine cancer. 42 1

The risk of developing endometrial cancer from post-menopausal estrogen use is discussed. Post-menopausal estrogen use has increased in Sweden from 4% to 8% of women 45-54 years of age between 1973 and 1978. Studies have shown that the risk of developing endometrial cancer increases after 3 years of estrogen treatment. In Sweden most post-menopausal estrogen treatment is prescribed for less than 3 years, and the estrogens are prescribed in dosages just high enough to avoid unwanted side effects. No definite causal relationship has been established between post-menopausal estrogen use and the increased incidence of endometrial cancer. A risk-benefit analysis weighs the benefits of post-menopausal estrogen treatment against possible risks. Estrogens should be prescribed in as low dosages and for as short a time as possible to avoid possible risks.
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PMID:[Postmenopausal estrogen and endometrial neoplasms]. 43 77

The most important short-term uses of estrogen are in the control of vasomotor disturbances, often called hot flashes, and in the therapy of athrophic vaginitis. Dosage should be as low as possible and on a cyclic basis. Estrogens can be employed cyclically but for an unpredictable term in the case of hypogonadism, female castration, and especially in the treatment of osteoporosis. The synthetic estrogen diethylstilbestrol (DES) is used as a contraceptive after coitus, in a large dose and within 72 hours, since it inhibits implantation of the fertilized ovum in the uterus. The use of estrogens in controlling some of the emotional conditions prior to menopause is not advisable, but they can be helpful in controlling acne and to arrest uterine bleeding. Conversely, estrogens have been shown to be associated with vaginal adenosis, and with clear cell carcinoma in girls whose mothers had been given DES during pregnancy; also with endometrial carcinoma in postmenopausal women who had taken the drug for years. The association between estrogens and breast cancer is still not clear, since the drug produces different results in different patients. Since estrogens increase blood coagulability their use is associated with an increased risk of thromboembolism and cardiovascular accidents. In prescribing estrogens physicians must evaluate each patient carefully, and require regular visits at six month intervals.
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PMID:Estrogens: their function, uses and hazards. Part 2. 62 3


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