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

Estrogen (ER) and progesterone receptors (PR) in tumorous mammary gland tissues have been investigated for a long time. The clinical significance of measuring the amount of ER and PR in the normal and pathological endometrium and myometrium was assessed. Endometrial and myometrial tissue obtained by operation was placed in a vessel containing liquid nitrogen an dry ice. Homogenization was performed at 15, 5, and 45 seconds in a buffer solution. After ultracentrifugation at 105 g for 1 hour, cytosol fraction was separated and used for ER, PR, and protein analysis according to the method of Lowry. The ER content of normal endometrium was 4 times higher than that of normal myometrium, however, the PR content in normal endometrium was only 2 times higher than in normal myometrium. The ER content did not differ in cancerous endometrium, but the PR content decreased 1.5 times. ER and PR amounts in myomatous neoplasm tissue increased 3 times compared with healthy myometrium. Robel et al. showed the ER increased to 6000-10,000/cell after ovulation, while the number of PR reached 14,000/cell in the preovulation phase. IN 29 endometrial cancer patients a significant decrease of both were fund. The ratio of PR to ER was 7.9 in the endometrial tissues of healthy women compared with 2.28 in those with endometrial cancer. In the present investigation, the respective ratios were 3.6 and 1.8; this low index was attributed to women in postmenopause without estrogen stimulation. The number of PR seems to be directly influenced by estrogens being higher in women with cyclical activity of the ovaries, thus receptors in uterine tissue change depending on endocrine functions. Endometrium and myometrium are hormone-dependent tissues. The increase of Er and PR is characteristic of benign processes, while the decrease of PR and especially of the PR/ER index indicates the malignant nature of the disease.
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PMID:[Clinical significance of analysis of estrogen and progesterone receptors in human uterine tissues]. 189 75

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

Estrogen receptors (ER) were examined in cytosol, nuclear potassium chloride (KCl) extractable fraction, and nuclear KCl unextractable fraction by the dextran-coated charcoal adsorption method in various gastric cancer tissue. The overall ER-positive rate in the cytosol and nuclear fraction was 19.2%. The maximum binding site (Bmax) was 36.0 to 175.0 fmol/mg of protein, and the dissociation constant (Kd) was 0.6 to 1.6 X 10(-9) in cytosol fraction. In the nuclear fraction, Bmax was 7.5 fmol/mg of DNA and Kd was 2.3 X 10(-9). Estrogen receptors were characterized in cytosol protein. In cytosol, the estrogen (E2)-ER complex was sedimented at approximately the 5S and 8S regions by 5% to 20% linear sucrose gradient centrifugation. A steroid specificity study of ER showed the presence of an binder in gastric cancer tissue. In conclusion, these results that gastric cancer tissue has E2 binding sites with the same biochemical characteristics as in breast cancer and endometrial cancer strongly suggest the hormonal dependency of gastric cancer.
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PMID:Characterization of estrogen receptor in human gastric cancer. 207 Mar 29

A North American case control study of 521 women under 45 years of age with breast cancer and 521 matched controls showed that incidence of oral contraceptive (OC) use prior to the birth of their 1st child was almost equal for both groups. It was also the same for those under 25 years of age (both cases and controls). A longitudinal study of 121,964 US nurses (592 of whom developed breast cancer) did not find increased risk for breast cancer among OC users. The age of first OC use was not significant. Another US study did not discover an association between OC use and breast cancer in women who had earlier had benign breast disease. In Scandinavia, a case control study of 422 women with breast cancer and 722 controls revealed a significant association between duration of OC use and breast cancer risk. The risk factor increased 2-fold after 7 years of OC use. A UK case control study of 755 women with breast cancer and 755 matched controls found a significant association between OC use and breast cancer risk. A UK longitudinal study showed a significant positive association between cervical cancer incidence and duration of OC use even when the researchers removed OC users who used barrier methods. OC users were less likely to have ovarian and endometrial cancer, however. Yet OC use was greatly related to death from all genital tract cancers. The discrepancy between the North American and European studies suggests that nurses should screen all women using OCs or wishing to use OCs for cancer risks which include known or suspected breast or reproductive tract cancer and abnormal vaginal bleeding. They must inform OC users of the association between genital infection and cervical cancer. They must advise OC users not in a monogamous relationship to use a barrier method. Estrogen doses in OCs while lower today than 30 years ago, are associated with cancer risk.
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PMID:Update on cancer risk and oral contraceptives. 210 27

The clinical use of estrogens and progestogens for menopausal women is reviewed, discussing the indications, results of studies on effectiveness of various agents o each target organ, contraindications, risk-benefit ratio, and types of drug preparations available and used in European countries. The indications for menopausal hormone replacement are primarily to prevent myocardial infarction and osteoporosis, and also to treat early menopause, urogenital atrophy, and severe skin, mucous membrane and psychic disorders. Mechanisms of action of estrogens and progestins, and anticipated results are detailed for each of the indications. Contraindications typical of oral contraceptives usually do not apply for hormone replacement. For example, only severe acute liver disease, current thromboembolism, endometrial cancer other than I, and breast cancer within 3-5 years of primary treatment are contraindications. Neither cervical, ovarian or vulvar cancer, diabetes, varicose veins, hypertension, nor history of liver disease or thromboembolism are contraindications: in some cases progestins or transdermal estrogens are recommended. Estrogen side effects suggest overdosage. Progesterone or its derivatives rather than oral contraceptive progestins are prescribed. There is a clear benefit, comparing cost of medication to that of treating consequences of estrogen deficiency. The preparations currently used in Europe include oral micronized estradiol, conjugated estrogens, transdermal patches, local vaginal estrogens, and injectable estradiol esters for those who cannot tolerate oral or transdermal agents. Preparations should contain progesterone unless the woman has had a hysterectomy. Combinations designed to avoid withdrawal bleeding are available.
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PMID:Clinical use of oestrogens and progestogens. 221 69

Estrogen therapy is extremely effective in relieving menopausal symptoms such as hot flushes, night sweats, urogenital atrophy and certain psychological symptoms. The short term side effects from this therapy are usually mild and self-limiting. They are more common in women who commence hormone replacement therapy some years after the menopause than in those who start treatment at about the time of the ovarian failure. Pre-existing gynaecological conditions such as fibroids and endometriosis can be worsened by estrogen therapy. The majority of published studies suggest a beneficial effect of postmenopausal estrogen therapy on cardiovascular and cerebrovascular disease. These effects may be mediated by favourable changes in lipids, but other mechanisms may also be involved. It is uncertain whether the adverse changes in lipids caused by progestogen therapy will reduce any of the benefits of estrogen therapy on the cardiovascular system. Osteoporosis is the major bone disease of the Western world; long term estrogen therapy will prevent its development in most postmenopausal women. The risk of endometrial carcinoma is increased with unopposed estrogen therapy; this increased risk appears to be abolished if a progestogen is added at an adequate dose and duration for each cycle. The risk of ovarian or cervical cancer is not increased with estrogen therapy. There may be an increased risk of breast carcinoma with long term postmenopausal estrogen use, but the studies show inconsistent results.
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PMID:A risk-benefit assessment of estrogen therapy in postmenopausal women. 222 68

To examine the relationship between exogenous estrogen administration and endometrial cancer, we used data from the Cancer and Steroid Hormone Study, a multicenter, population-based case-control study. Estrogen replacement therapy for greater than or equal to 2 years was associated with an increased risk of both localized and extrauterine cancer (relative risk = 2.8, 95% confidence limits 1.6, 4.6; relative risk = 2.9, 95% confidence limits 0.9, 9.4, respectively). However, the latter finding was based on a small number of cases in which estrogen was used. Women who underwent estrogen replacement therapy for greater than or equal to 2 years had significantly elevated risks of endometrial cancer (2.1 for 2 to 5 years and 3.5 for greater than or equal to 6 years). An elevated risk persisted for greater than or equal to 6 years after discontinuation of therapy. Women who exclusively used conjugated equine estrogen preparations less than or equal to 0.625 mg had no increased risk of endometrial cancer. A history of oral contraceptive use appeared to reduce the risk of endometrial cancer associated with estrogen replacement therapy. However, these latter two potentially important findings were based on a small number of cases in which hormones were used.
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PMID:Estrogen replacement therapy and the risk of endometrial cancer: remaining controversies. 230 83

Estrogen (ER) and progesterone (PgR) receptor values in 105 endometrial carcinomas were compared using immunocytochemical and standard biochemical techniques. Peroxidase-antiperoxidase staining for location of anti-ER (H222) and anti-PgR (JZB39) primary antibodies was used to generate a semiquantitative (HSCORE) assessment of receptor content in tissue components and the total specimen. Both total HSCORE and cancer component HSCORE correlated with log biochemical assay values for ER and PgR. Biochemical assay values, total HSCORE, and cancer component HSCORES all demonstrated internal correlations between ER and PgR levels. Correlation was somewhat closer for cancer component HSCORE values of ER and PgR than the values for total tissue HSCORE. When receptor content was analyzed by histologic grade, all three estimates of receptor status demonstrated a decreasing proportion of ER and PgR positive lesions with decreasing histologic differentiation; however, the proportion of receptor negative lesions in grade 3 lesions was much higher when using total HSCORE or cancer component HSCORE than when using biochemical assay values (P less than 0.005. Immunocytochemical techniques for localization of ER and PgR in endometrial carcinoma specimens may allow a more focused evaluation of the receptor content in the malignant elements than standard biochemical techniques.
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PMID:Estrogen and progesterone receptor content of endometrial carcinomas: comparison of total tissue versus cancer component analysis. 231 45

UM-EC-2 was established from a patient with poorly differentiated stage IB endometrial carcinoma. This cell line produces tumors in nude mice that have the same histological features as the patient's tumor. UM-EC-2 cells express b2-microglobulin, the epidermal growth factor receptor (EGF), and the H blood group antigen. This membrane antigen phenotype is consistent with cells of human endometrial origin. The karyotype of UM-EC-2 is fairly complex, with rearrangements affecting all chromosomes except 3, 10, 14, 19, and 20. There were two populations of cells, a hyperdiploid population with a modal number of 53-55 and a hypertetraploid population with a modal number of 109. A postulated sequence of events before and after tetraploidization is suggested based on the number of copies of individual chromosomes and rearrangements. Comparison of the UM-EC-2 karyotype to that of UM-EC-1 (a previously described line from a different patient with endometrial carcinoma) revealed that the two lines share eight very similar chromosome changes, which include loss of most of chromosome 4, breakpoints affecting proximal bands on 8p, loss of most of 9q, a breakpoint at 12q22, loss of 13q, breakpoints in proximal bands on 18q, and a breakpoint at 22p11. These changes may represent nonrandom chromosome abnormalities in poorly differentiated endometrial cancer. Estrogen (ER) and progesterone (PgR) receptors were not detected in either the primary tumor or the cell line. Nevertheless, UM-EC-2 cells were very sensitive to growth inhibition by tamoxifen (TAM) in vitro. One micromolar TAM caused 50% inhibition of cell growth, 2.5 microM caused cytostasis, and 5 microM TAM was cytotoxic, killing all cells after 5-7 days of exposure to the drug. Paradoxically, 100 nM estradiol (E2) caused a moderate increase in the growth of the cells but it did not prevent or reverse growth inhibitory effects of TAM. These findings support the concept that in some tumors TAM causes growth inhibition by an ER-independent mechanism. UM-EC-2 cells were also sensitive to growth regulation by EGF. Thus, these cells provide a new in vitro model of human endometrial cancer in which the roles of both TAM and EGF as growth regulatory substances can be investigated.
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PMID:Establishment and characterization of UM-EC-2, a tamoxifen-sensitive, estrogen receptor-negative human endometrial carcinoma cell line. 234 64

The records of 16 patients with an obstructed, fluid-filled uterus due to carcinoma of the uterus or to its treatment by radiation therapy were analysed. In 12 uteri the presence of malignant tumor was simultaneously established, e.g. primary cervical carcinoma (1), recurrence of cervical (4), endometrial Stage II or III carcinoma (2), second primary tumors, MMT (2), and endometrial carcinoma (3). The uterine fluid consisted of blood (8), pus (3) or was serous (3). Twice the fluid could not be analysed. In our series the prognosis of patients with recurrent cervical cancer or a second primary tumor was poor. Improvement of the prognosis can result by intensifying the follow-up examinations with CT and/or ultrasound in the first 2 years, and not by prolongation of the follow-up period. Estrogen therapy was believed to be the causal factor in three cases of hemotometra. In the near future an increase of this complication is possible as a consequence of hormonal replacement therapy given to prevent osteoporosis after pelvic irradiation.
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PMID:Fluid detection in the uterus during and after irradiation for carcinoma of the cervix--clinical implications. 240 60


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