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

Some retrospective studies that have indicated an association between estrogen replacement therapy (ERT) and endometrial cancer are reviewed and critiqued in this brief article. In 1975, 1 report estimated that about 51% of women in menopause underwent some form of estrogen therapy. Estrogen therapy in high doses was first associated with endometrial cancer in rabbits more than 20 years ago. No association in humans was reported until 1975 when 2 retrospective studies reported ERT asso with increased incidence of endometrial cancer in postmenopausal women. In this study, 48% of cases vs. 17% of controls had used ERT. Calculated risk of developing the cancer was 4.5 times greater for users of estrogens. Another similar study reported that 57% of women diagnosed with endometrial cancer from 1970-1974 had received prior ERT. Only 15% of controls had ERT. This risk was calculated at 7.6 times for ERT users. A supporting study calculated increased risk at 8 times greater. Epidemiological studies have also suggested this ERT-endometrial cancer association. Some clinicians dispute these findings using several arguments, especially the fact that retrospective analysis cannot infer cause and effect. In addition, the studies have been criticized for nonclarity in regard to drug dosage and therapeutic regimen, mortality rate, percent of Grade 1 lesions, and whether or not endometrial biopsies were obtained before women started ERT. In addition, the studies have been confounded by the fact that women using ERT have had better follow-up with earlier detection of neoplastic changes.
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PMID:Estrogen replacement therapy and endometrial cancer: the elusive link. 689 48

In 49 carcinomas of the endometrium of varying clinical stages the estrogen and progesterone receptors were studied by charcoal absorption methods. The cases were studied between 1979 and 1981. 64% of the investigated cases were receptor positive, 35% were receptor negative. Estrogen receptors were detected in 61% and progesterone receptors in 49% of the cases. Both estrogen and progesterone receptors were detected in 45% of the cases. The receptor status was correlated with the clinical stage, the microscopic differentiation and the age of the patient. In 30 cases with a follow-up of more than 3 months it was attempted to determine the prognostic value of the steroid receptor status in endometrial carcinoma. The treatment possibilities with progestational agents and antiestrogens and with tamoxifen were discussed in view of the receptor status.
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PMID:[Estrogen and progesterone receptors in corpus uteri carcinoma and their clinical significance]. 692 60

411 patients suffering from endometrial carcinoma were seen at the Roswell Park Memorial Institure in Buffalo, New York, between 1970 and 1978. These patients were matched and compared with 338 controls having no neoplastic disease or neoplasms other than of the female genital tract. There was a significantly higher incidence of diabetes, hypertension, and obesity in the uterine cancer patients than in the controls. On the other hand, nulliparity or family history of uterine or other cancer could not be correlated with endometrial cancer in these patients. The control and cancer groups did not differ markedly in the use of estrogens for menopausal or gynecologic reasons. Estrogen use in oral contraceptives (OCs) and for uncertain or unknown reasons was higher in the control than in the cancer group. The uterine cancer group was slightly older (median age 64.2) than the control group (median age 59.7), but this difference is small and believed unlikely to account for the results described.
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PMID:Estrogens and endometrial cancer. 694 29

Estrogen has been used to induce a wide variety of tumors in various animal species but only the rabbit is reported to reliably develop endometrial carcinoma. Variables associated in humans with an increase susceptibility to endometrial adenocarcinoma include aging, obesity, liver diseases, polycystic ovary disease, and ovarian tumors. In women estrogen induces mitotic activity in the endometrium and promotes the proliferation of the endometrium. Current concern that estrogen replacement therapy in postmenopausal women may be associated with increased risk of endometrial adenocarcinoma is based on: 1) reports of increased incidence of the disease, and 2) epidemiologic studies associating estrogen administration with an increased risk of endometrial carcinoma. The author draws the following conclusions based on the existing data: 1) there is likely a small but significant increase in the risk of development of endometrial adenocarcinoma among menopausal women on estrogen replacement therapy; 2) the increase in risk appears to be greatest for women who do not have any of the constitutional stigmas that would ordinarily place them at higher risk for adenocarcinoma; 3) risk increases with increasing duration of therapy, probably following a latent period of undetermined duration; 4) risk increases with increasing dose of estrogen; 5) progestin administration likely affords some protection against the risk, but the potential risks of administering the hormonal equivalent of a combination oral contraceptive periodically to elderly women have yet to be examined carefully; and 6) careful surveillance of patient populations on estrogen replacement therapy may limit the risk of adenocarcinoma associated with estrogens to early, highly curable lesions. It is incorrect to assume that estrogen actually causes carcinoma of the endometrium; it more likely induces a precancerous hyperplastic state in a dose-related fashion and only certain individuals ultimately develop invasive carcinoma.
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PMID:Does estrogen cause adenocarcinoma of the endometrium? 701 37

Postmenopausal genital bleeding is a symptom that requires thorough evaluation. In most cases the cause is benign. Nongenital and nonuterine causes will be found occasionally and should be managed accordingly. The principal thrust of management involves thorough history, examination, and interpretation of endometrial histology. The latter is especially necessary to exclude the most significant, but not most common, cause of postmenopausal bleeding, i.e., adenocarcinoma of the endometrium. Estrogen therapy contributes to postmenopausal bleeding and is usually contraindicated in such cases. Endometrial hyperplasia is considered a precursor lesion to endometrial carcinoma, but the incidence of progression is not great. Thus a scheme of conservative management that relies on repeat histologic examination of the endometrium to determine the biologic potential of endometrial hyperplasia is recommended. Although hospital D&C of the uterus is the traditional accepted method of evaluating the endometrium, there are persuasive reasons to consider suction endometrial biopsy as an appropriate alternative in most patients presenting with postmenopausal bleeding.
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PMID:Management of postmenopausal bleeding. 701 38

The climacteric is an interval characterized by a multitude of physiologic, psychologic, and sociologic alterations that result in an individual's adaptation to life beyond reproduction. The common denominator of the physiologic changes is the loss of functional ovarian follicles and their ability to produce estradiol. The relative estrogen deficiency results in a myriad of systemic changes, some of which in themselves may impair the quality of life or be life-threatening. Estrogen replacement therapy is effective in alleviating some of these changes, including osteoporosis, vasomotor symptoms, and genital atrophy. This treatment, however, confers additional risks, endometrial adenocarcinoma being the one of greatest concern. This risk can be reduced by carefully selecting patients to be treated, closely following them, minimizing the duration and amount of exposure, and adding a progestin to the regimen. It is hoped that the risk of endometrial cancer and other adverse reactions associated with estrogen use can be further reduced when more data regarding optimum dosage and choice of agents are available.
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PMID:Endocrine problems in the menopause. 703 2

In order to determine the role of postmenopausal estrogen use in survival of patients with endometrial cancer, we identified, through a population-based tumor registry serving the area, all white women in King County, Washington, aged 50 to 74, who developed endometrial cancer between January, 1975, and April, 1976 (N = 363). Estrogen use prior to diagnosis and survival status were ascertained through personal interview, medical records of private physicians, and registry follow-up data. The 4-year relative survival ratio in estrogen users was 1.05 compared to 0.898 in nonusers. Overall, after adjustment for age, the survival in estrogen users was significantly better than in nonusers (chi 2 = 30.5; p much less than 0.0001). While estrogen use may predispose to an increased incidence of endometrial cancer, it appears that such use does not lead to increased mortality from this condition.
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PMID:Survival among women with endometrial cancer: a comparison of estrogen users and nonusers. 709 Dec 28

Interviews concerning prior use of oral contraceptives (OCs) were conducted among female residents of King and Pierce Counties in the state of Washington in whom endometrial cancer was diagnosed during 1975-1977. Their responses were compared with those of a random sample of women from the same population. Women who had taken Oracon (0.1 mg of ethinyl estradiol and 25 mg of dimethisterone) were estimated to have a risk of endometrial cancer of 7.3 times that of other women (P=0.007). This elevation in risk was not observed in users of other sequential preparations. Women who had used combined OCs had only 50% of the incidence of endometrial cancer of nonusers, although the protective effect was not evident among those who subsequently took menopausal estrogens for more than 2 years. It is likely that the use of Oracon predisposed women to the development of endometrial cancer. THese associations suggest that development of neoplasis in the endometrium can be very sensitive to hormonal factors. If an OC, like Oracon, emphasizes the estrogenic component, promotion of cancer can be the result. If, like combined preparations, the contraceptive emphasizes the progestational component, protection against cancer can be the result.
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PMID:Incidence of endometrial cancer in relation to the use of oral contraceptives. 735 90

The exemplary study of Weiss and Sayvetz of the risk of endometrial cancer among oral contraceptive (OC) users is reported. The only study limitation is that the cases available were too few to provide highly precise estimates of all the associations seen. Yet the study did show that women who took the sequential drug Oracon have a risk of endometrial cancer that is appreciably higher than that of women who did not take OCs. The study also provides some evidence that the combined drugs do not increase the risk of endometrial cancer and that they might actually be protective. The study can only suggest that other sequential drugs are not as harmful as Oracon and that they may even be protective like the combined drugs. Oracon differed from all other OCs in 3 ways, and each contributed to making it the most estrogenic: 1) only Oracon used the weak progestogen dimethisterone; 2) only Oracon supplied 100 mg daily of the estrogen ethinyl estradiol; and 3) Oracon's monthly sequence included 16 days of estrogen alone while other sequential drugs included 14 or 15 days, and the combined OCs have no estrogen-only day. The finding of Weiss and Sayvets that, if accurate, will prove to be of greatest importance is the apparent anticarcinogenic effect of combined oral contraceptives.
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PMID:Oral contraceptives and endometrial cancer. 735 94

Clinical and pathologic findings were compared in 43 postmenopausal endometrial carcinoma patients who had received exogenous estrogens prior to diagnosis and 79 similar patients unexposed to estrogens. Estrogen non-users were more likely to manifest lower parity, later menopause, obesity, hypertension, and diabetes, all of which have been considered to be constitutional risk factors for the development of endometrial carcinoma. Although estrogen users and non-users had similar extent of disease as judged by clinical stage, there was a tendency to more myometrial invasion in hysterectomy specimens from non-users, as well as greater frequency of unfavorable histologic types and grades of tumor. At short-term follow-up, more recurrences occurred in non-users, and this tendency appeared to be independent of clinical stage, histologic type, histologic grade, or modality of treatment. The significance of these and other observation to the determination of the risk-benefit ratio for estrogen administration is discussed.
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PMID:Endometrial carcinoma: clinical-pathologic comparison of cases in postmenopausal women receiving and not receiving exogenous estrogens. 738 46


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