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

The medical profession has been disturbed and bewildered by a number of recent communications which discussed a possible relationship between contraceptive sequential therapy and the incidence of endometrial cancer and between the postmenopausal application of conjugated oestrogens and endometrial carcinoma. An analysis of these reports is made critically and in detail and supplemented with observations on the risk of carcinoma of the breast. The practical aspects are delineated and a precise guide to postmenopausal oestrogen therapy presented.
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PMID:Oestrogens and endometrial cancer: a point of view. 19 6

Despite many years of extensive investigation, there has been neither a clear-cut pattern of hormonal production nor milieu found in women with breast cancer. Estrogen replacement therapy for menopause does not significantly increase the risk of breast cancer and one study indicated that estrogen users have a lower incidence of breast cancer than that observed in untreated women. Some studies have shown that the mortality rate from breast cancer is lower in estrogen-treated postmenopausal women. Only one investigator has found any significantly increased risk of breast cancer in oral contraceptive users. In that report, increased duration of birth control pill use decreased the risk of breast carcinoma. Several studies were unable to find an increased risk of breast cancer from oral contraceptives while one investigation observed a lower incidence in birth control pill users than that expected. The mortality from carcinoma of the breast in oral contraceptive users was lower than in non-users, most likely due to earlier detection. Although some retrospective studies have indicated that estrogen use increases the risk of endometrial cancer, a prospective investigation found only an insignificant increase. Progestogens afford some protection from cancer in estrogen-treated postmenopausal women. The incidence of endometrial adenocarcinoma is lower than that observed in untreated postmenopausal women. Combination oral contraceptives are protective against developing adenocarcinoma of the endometrium but sequential birth control pills may afford less protection.
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PMID:The role of hormones in the etiology of breast and endometrial cancer. 29 15

The concentration of carcino-embryogenic antigen in the serum of healthy women and of patients with different benign and malignant genital tumors was determined before and after treatment. The carcino-embryogenic antigen was elevated to more than 2.5 ng/ml in 11% of the healthy control patients. Patients with carcinoma of the breast had positive CEA tests in 60%. Patients with ovarian cancer had positive CEA tests in 57%, women with carcinoma of the uterine cervix had positive tests in 50% and women with endometrial carcinoma had increased CEA levels in the serum in 38% of the cases. Following treatment the CEA values decreased.
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PMID:[Carcino-embryogenic antigen (CEA) in patients with genital tumors (author's transl)]. 88 32

The metabolic effects of sex steroids pertinent to cardiovascular risk are described. These effects are discussed for estrogen inducible proteins, coagulation and fibrinolysis, blood pressure and hypertension, carbohydrate metabolism, lipids and lipoproteins, and vessel walls and local prostaglandins. Also described is the cardioprotection from estrogens and estrogen/progesterone treatment and cardiovascular risk. Oral contraceptive (OC) and cardiovascular risk are also discussed with the following effects identified: the influence on many of the multiple risk factors involved in the development of cardiovascular diseases (i.e., lipids, carbohydrate metabolism, and hemostasis), an association between OC use and thromboembolic accidents, a state of hypercoagulability counterbalanced by increased fibrinolytic activity, venous thrombosis, a relationship with the dosage of androgenic progestogens. no atherogenic origin, no age limit for prescribed, healthy, nonsmoking women, and an increased peripheral insulin resistance. It is concluded that it is rarely inadvisable to prescribe low dose natural estrogens in postmenopausal hormone replacement therapy. Factors contraindicating such use are undiagnosed genital bleeding, an active thrombolic or cardiovascular process, carcinoma of the breast or endometrium, and acute liver failure. Estrogen replacement therapy may exert some cardioprotective effect. When progestogens are added to prevent endometrial carcinoma development, the benefits might be reduced. Low estrogen and low progesterone OC use among healthy, nonsmoking women even in middle age poses no risk of death from cardiovascular disease. Premenopausal women may even be protected from coronary atherosclerosis with estrogen-containing OCs. However, it is advisable that OCs be used with the least possible impact on lipid and carbohydrate metabolism, as well as on hemostasis. For those with some prior cardiovascular risk, there are theoretical advantages at present for use of the new, less, or nonandrogenic progestins in OCs; however, caution is urged and informed consent must be obtained until epidemiological studies support this position.
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PMID:Sex hormones and cardiovascular risk. 192 64

We report the very unusual observation of an 85-year-old woman who developed five different tumors in distinct sites over a 12-year period. These tumors were, in the following order of appearance, an infiltrating lobular carcinoma of the breast, an endometrial carcinoma with an ovarian granulosa cell tumor, a clear cell adenocarcinoma of the kidney, and a urothelial carcinoma of the bladder. Two factors may have been involved in the genesis of the multiple carcinomas in this patient, i.e. a hormonal factor (hyperestrogenemia) and radiotherapy.
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PMID:[Multiple cancers: a case with 5 different tumors]. 275 62

Progestogens should be added to estrogen replacement therapy, not only to prevent endometrial cancer in women with a uterus, but also to reduce the risk of breast cancer in some women. Smoking should be discouraged to reduce the risk for both lung cancer and heart disease. Recommendations should be made to increase fiber intake to lessen the risk for carcinoma of the colon. Reducing fat intake also decreases risk for colon cancer, as well as carcinoma of the breast. Postmenopausal bleeding must be investigated for early diagnosis of endometrial cancer and, when endometrial hyperplasia is the finding, it should be treated with progestogens to prevent adenocarcinoma. The progestogen challenge test is recommended for all women with a uterus, and if bleeding occurs, the progestogen should be continued for 13 days each month. Use of mammograms and other diagnostic modalities should be increased to make the earliest possible diagnosis of breast cancer.
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PMID:Cancer in the older woman: diagnosis and prevention. 304 28

Hormones, particularly estrogens, have been suspected for many years of being carcinogens. Retrospective studies from the mid-1970s indicate that unopposed estrogen replacement therapy increases the risk for endometrial cancer. However, recent reports have failed to incriminate even unopposed estrogens for any significantly increased risk of breast cancer. Added progestogen, in proper duration and dosage, almost completely negates the estrogen-increased risk for adenocarcinoma of the endometrium. There is increasing evidence that progestogen added to estrogen replacement may decrease the risk for carcinoma of the breast in some women.
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PMID:Sex steroids and cancer. 330 19

During a follow-up of 665 patients with carcinoma of the breast age 40 years or older, 46 developed a second primary carcinoma of the opposite breast and 30 developed a nonmammary malignancy (median FU = 6 yrs). Comparing our number of observed cases with the number of expected cases (calculated from the female age-specific incidence rate of the data of the Surveillance, Epidemiology and End Results (SEER) and from the actual cumulative person-years of follow-up), our patients with breast cancer did not have higher probability of developing additional nonmammary malignancy, but did have over five times the chance of developing a second breast cancer as other females to have any such cancer. Comparing the distribution of specific sites of our nonmammary second cancer with that reported by the SEER's study, the proportions of patients with colorectal, lung cancer, and lymphoma were similar. But we did see relatively more carcinomas of the uterine cervix, ovary, vulva, sarcoma, and stomach/duodenum, and fewer carcinoma of the endometrium. These differences could be explained by our small series, patient characteristics, and selected referral pattern.
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PMID:Additional malignant neoplasms in patients with breast carcinoma. 372 72

Determination of the tissue concentration of hormone receptors in gynaecological malignancies has achieved a great importance over the past few years. In carcinoma of the breast this not only constitutes an excellent prognostic parameter, receptor-positive cases usually having a much better prognosis, but also reliably predicts the response to endocrine treatment: the higher the receptor concentration, the higher the remission incidence under hormonal treatment. With regard to the response to chemotherapeutic treatment the predictive value of receptor determinations is still a matter of dispute. In both carcinoma of the breast and carcinoma of the endometrium there is a good correlation between the degree of differentiation and the concentration of receptors. Since the response to treatment with progestational agents depends on the concentration of progesterone receptors, induction of this receptor by means of antioestrogenic medication can be used therapeutically. In ovarian carcinoma a similar distribution of hormone receptors is found. Whether receptor concentration in ovarian carcinoma is related to prognosis and response to endocrine treatment is still under investigation. It can be assumed that determination of hormone receptor concentrations will become an integral part of the management of gynaecological malignancies.
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PMID:[The importance of hormone receptor analysis for diagnosis and therapy of gynecologic malignancies]. 631 Sep 2

There are an estimated 8-10 million oral contraceptive (OC) users in the U.S. Investigation of the effects of OCs on neoplasia is not easy; currently 4 investigative methods are used: 1) case reports, 2) disease rate and trends, 3) case-control studies, which are the main source of careful retrospective information, and 4) cohort studies, which compare the incidence of disease in patients exposed to suspected environmental factors, and in those who are not exposed. Major risk factors for carcinoma of the breast are female sex, age, genetic predisposition, previous benign breast disease, and previous cancer of one breast; undetected breast cancer may be present for many years before diagnosis, and risk is increased in patients with chronic cystic mastitis or fibrocystic disease of the breast. Clinical observations have suggested a strong association between endocrine influence and the incidence or progression of breast cancer; current evidence tends to support the role of estrogens in the etiology of carcinoma of the breast with respect to long-term estrogen administration, but this evidence is not valid for young patients who are on combined OCs. Most studies have documented a decreased risk of benign breast disease with length of OC use persisting for 4 years; these studies, however, did not analyze lesions by histologic type. Studies that show a protective effect on benign disease do not show the same protective effect for breast cancer. Data from cohort studies show no association of OCs with breast cancer. Since 1972 a number of reports have associated OCs with liver tumors, stating that risk increases with duration of use. A national survey revealed that the frequency of malignant tumors increased with age, but that the frequency of benign lesions had a peak in the 26-30 age group which corresponds to increased use of OCs. Benign tumors are dangerous because they tend to rupture spontaneously. The association between pituitary adenoma, causing postpill amenorrhea, and OC use is very controversial. OC use may also cause endometrial hyperplasia; postmenopausal estrogen use has also been associated with endometrial carcinoma, although the causal relationship has never been proven; progestogens may be useful in the therapy of some endometrial carcinomas. Carcinoma of the cervix seems to be more influenced by age at 1st intercourse and by multiple sexual partners than by OC use; several case-control studies have shown that there is no significant difference between incidence among OC users and nonusers. Data about the association between OCs and ovarian carcinoma are reassuring but incomplete. OCs should not be used in patients with positive chorionic gonadotropin titers who have been treated for hydatidiform mole.
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PMID:Neoplasia and hormonal contraception. 702 11


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