Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

E.F. Diamond questions the use of DES (Diethylstilbestrol) as a method of pregnancy prevention after rape because of the increased risks of vaginal cancer in women exposed to DES in vitro; the relationship to congenital anomalies and to endometrial carcinoma; and the actual number of pregnancies resulting from rape. According to Diamond, studies have shown that an insignificant number of pregnancies occur because of rape and to support this claim he cites a study conducted in Minnesota where 4,000 rapes resulted in 0 pregnancies. Diamond also assails the Catholic health care institutions which permit the use of DES as a postcoital contraceptive claiming that they are in actuality performing early abortion by medication.
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PMID:Physician notes hazards of DES use to prevent pregnancy. 63 11

The sex steroid hormone receptor levels of uterine cytosol were assayed in the course of experimental induction of endometrial carcinoma in rats. Effects of administration of various hormones on the receptor levels were examined with each histological pattern of endometrium. 1) The dissociation constants for E2 and R5020 bindings with uterine cytosol were almost fixed in spite of various histological patterns of endometrium. 2) The influence of administrated hormones on the receptor assay system could be neglected by the preincubation of uterine cytosol with DCC for five times. 3) By the administration of DES for six weeks, estrogen receptor levels were increased significantly in adenocarcinoma, while progesterone receptor levels did not show the tendency of decreasing. 4) By the administration of MPA combined with DES, estrogen receptor levels were not decreased significantly in both atypical adenomatous hyperplasia and adenocarcinoma; progesterone receptor levels were decreased in all groups. 5) By the administration of MPA, estrogen receptor levels were decreased significantly in adenocarcinoma. These data suggest that receptor levels can be controlled by the administration of sex hormones in the course of development of endometrial carcinoma.
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PMID:[Changes of sex steroid hormone receptors in rat uterine cytosol during experimental induction of endometrial carcinoma (author's transl)]. 645 22

This is a general discussion of commonly seen oncology problems in gynecology for the general practitioner and the nongynecologic specialist. Vaginal, cervical, ovarian, and endometrial cancer are discussed. Studies have shown a possible relationship between perinatal exposure to DES(diethylstilbestrol) and clear cell adenocarcinoma of the vagina and cervix in young women. Of the more than 350 reported cases of this previously rare disease, 2/3 had a history of in utero exposure to DES. 80-90% of all exposed women show adenosis of the vagina. There is no evidence, however, that it is a precursor of cancer and no examples of the progression have been cited. All DES-exposed daughters should have yearly PAP smears and iodine staining or colposcopy of the vagina. The American College of Obstetricians and Gynecologists differs from the American Cancer Society in recommending yearly PAP smears to detect cervical cancer. There is no risk and no morbidity with the smear. Only the cost is a consideration. Endometrial cancer accounts for 7% of all cancers in women, occurring in 2.2% of all women. Survival rates with this type of cancer are 68% at 5 years. Some studies have implicated the use of postmenopausal estrogens with the etiology of endometrial cancer. Any abnormal bleeding should be checked. Ovarian cancer presents in more advanced stages and has a survival rate at 5 years of only 25%. Surgery and chemotherapy are the prescribed treatment for each of these cancers.
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PMID:Gynecological malignancy. 724 64

In the Diethylstilbestrol [DES] Combined Cohort Follow-up, the age- and calendar-year specific standardized incidence ratio [SIR] for clear cell adenocarcinoma [CCA] was 27.6 (95% confidence interval [CI] 7.51-70.6) for the exposed women. The SIR for breast cancer was 1.17 (95% CI 1.01-1.36) and the hazard ratio [HR] adjusted for birth year and cohort for comparison with the unexposed was 1.05 (95% CI 0.79-1.41). The SIR for pancreatic cancer was 2.43 (95% CI 1.21-4.34) and the adjusted HR for comparison with unexposed women was 7.16 (95% CI 0.84-61.5). There was little evidence of excess risk for other sites. There appeared to be a deficit in risk for endometrial cancer among the exposed (SIR 0.61; 95% CI 0.35-0.98), and an excess in the unexposed (SIR 1.55; 95% CI 0.95-2.40); the adjusted HR was 0.45 (95% CI 0.22-0.93) for the internal comparison. There was no overall excess cancer risk in exposed women compared with general population rates (1.06; 95% CI 0.95-1.17) or with unexposed participants (adjusted HR 1.03; 95% CI 0.84-1.25). These data do not support the suggestion that there is a diathesis of cancers in DES exposed female offspring The excess risk of breast and pancreatic cancers that we observed is concerning and warrants continued follow-up and mechanistic investigation. Environ. Mol. Mutagen. 60:395-403, 2019. Published 2017. This article is a US Government work and is in the public domain in the USA.
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PMID:Prenatal diethylstilbestrol exposure and cancer risk in women. 2912 79