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

Morning serum steroid levels were determined in postmenopausal chronic smokers and nonsmokers. Postmenopausal smokers (n = 9) had significantly elevated levels of cortisol, progesterone (P), 17-hydroxyprogesterone (17-OHP), androstenedione, and testosterone compared with nonsmokers (n = 16). The increases were most significant for cortisol (P less than 0.001) and 17-OHP (P less than 0.0005). Estrone, estradiol, dihydrotestosterone, and dehydroepiandrosterone sulfate did not differ between the groups. P to estrogen ratios tended to be higher in the smoking population. The significantly elevated P levels observed in the group of postmenopausal smokers may explain, in part, the epidemiologic finding that women smokers have a decreased incidence of endometrial carcinoma. In addition, the hypercortisolism associated with smoking may increase the risk of osteoporosis.
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PMID:Serum steroid hormone profiles in postmenopausal smokers and nonsmokers. 295 Dec 78

An antiestrogenic effect of cigarette smoking has been suggested, principally on the basis of data on premenopausal women. We examined the relation between cigarette smoking and endogenous sex-hormone levels in a population of 233 white, postmenopausal women 60 to 79 years of age. Current cigarette smokers had significantly higher mean plasma levels of the adrenal androgens dehydroepiandrosterone sulfate and androstenedione than nonsmokers. Mean levels for smokers and nonsmokers were 3.1 mumol per liter (116 micrograms per deciliter) and 2.3 mumol per liter (86 micrograms per deciliter), respectively (P less than 0.001), for dehydroepiandrosterone sulfate, and 27.8 nmol per liter (797 pg per milliliter) and 22.5 nmol per liter (643 pg per milliliter), respectively (P = 0.002), for androstenedione. A dose-response relation was apparent for these hormones; mean plasma levels increased concomitantly with cigarette consumption. The differences in hormone levels remained after adjustment for age and body-mass index. Mean levels of estrone, estradiol, testosterone, and sex-hormone-binding globulin did not differ between smokers and nonsmokers. These results suggest that the possible decreased risk of breast and endometrial cancer associated with cigarette smoking may not be mediated through lower levels of endogenous estrogen, at least in postmenopausal women, and they raise questions about the role of androgens in disease mechanisms in older populations.
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PMID:Cigarette smoking and levels of adrenal androgens in postmenopausal women. 296 32

A nude mouse model for the growth of human endometrial carcinoma and hormonal modulation of the progesterone receptor (PR) was established previously. This study describes the effect of 17 beta-estradiol and tamoxifen (TAM) on growth rate and PR concentration in a hormonally responsive human endometrial tumor (EnCa 101) grown in this experimental system and presents the first characterization of human endometrial carcinoma PR. EnCa 101 was transplanted subcutaneously into ovariectomized, BALB/c, nu/nu athymic mice and grown under 17 beta-estradiol-stimulated, TAM-stimulated, and control conditions. Both 17 beta-estradiol and TAM increased the growth rate of EnCa 101 in nude mice, and a parallel increase in the cytosol PR concentration was observed, from 130 +/- 55 (SD) fmol/mg protein to 1,311 +/- 598 fmol/mg protein and 710 +/- 310 fmol/mg protein, respectively. PR was partially purified by phosphocellulose and DEAE cellulose chromatography, and the DEAE eluate was analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and photoaffinity labeling with [17 alpha-methyl-3H]promegestone ([3H]R5020). Two PR-negative tumors (EnCa K and EnCa V) were also examined in parallel. Coomassie blue staining of gels revealed that the protein patterns of all of the partially purified preparations from EnCa 101, EnCa K, and EnCa V were essentially identical. In contrast, photolabeling and sodium dodecyl sulfate-polyacrylamide gel electrophoresis of EnCa 101 grown in the presence of 17 beta-estradiol or TAM revealed incorporation of [3H]R5020 into proteins of molecular weight approximately 116,000 and 85,000. Labeled proteins of molecular weight 66,000, 45,000, and 35,000 were also observed. In each case, the labeling was competable with excess non-radioactive R5020. No incorporation of [3H]R5020 was observed in EnCa 101 grown in the absence of estrogen, nor was any observed in EnCa K or EnCa V.
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PMID:Photoaffinity labeling of the progesterone receptor from human endometrial carcinoma. 405 15

Thirteen postmenopausal women with benign endometrial changes including proliferative, secretory and polypous endometrium, endometrial hyperplasia and atypia (group I) and 13 randomly selected age-matched controls with normal atrophic endometrium (group II) were studied with respect to serum levels of dehydroepiandrosterone (DHA) and its sulfate (DHAS), testosterone, total estrone, estradiol-17 beta, progesterone, FSH and prolactin. Serum levels of DHA, DHAS, testosterone and total estrone were significantly higher in group I than in group II; otherwise no significant differences were found. Mean values for body weight and for Broca's index, respectively, were almost identical in the two groups. It is speculated that the adrenal androgens may affect the endometrium in two ways, viz. via peripheral conversion to estrogens and/or via direct interaction with endometrial steroid receptors. The results give further support to the hypothesis of an association between adrenocortical hyperactivity and endometrial abnormalities including endometrial carcinoma.
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PMID:Peripheral hormone levels and the endometrial condition in postmenopausal women. 622 73

The metabolism of [3H] estrone sulfate was studied in endometrial tissue obtained from postmenopausal women with atrophic endometrium (I), benign endometrial proliferative changes (II) and endometrial carcinoma (III) and in perimenopausal women with proliferative (IV) and secretory (V) endometrium. Total hydrolysis (i.e. formation of [3H] estrone + [3H] estradiol-17 beta) of [3H] estrone sulfate as well as formation of [3H] estradiol-17 beta only was significantly less in group I than in the other groups. The formation of [3H] estradiol-17 beta was greater in group V than in the other groups. It is speculated that formation of estradiol-17 beta in the endometrium from estrone sulfate may be of importance in the genesis of endometrial disorders in the postmenopausal woman.
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PMID:Metabolism of estrone sulfate in human endometrium. 666 65

Estrogen metabolism was studied in a newly established cell line (RL95-2) derived from a human endometrial carcinoma. Estradiol and estrone were metabolized to water-soluble derivatives by cells under in vitro culture conditions. Between 80-90% of the added steroids were metabolized, with nearly quantitative recovery of the products from the incubation medium. Arylsulfatase treatment converted the metabolites to ether-soluble forms, whereas beta-glucuronidase had no effect on the aqueous solubility of these compounds. Butanol extracts of the water-soluble estradiol metabolites cochromatographed on high performance liquid chromatography with 17 beta-estradiol-3-sulfate (93.6%) or estrone-3-sulfate (3.5%). No more than 6% of the estradiol added to the incubation medium was recovered in the form of estrone, either as estrone or estrone sulfate. After arylsulfatase treatment of the estradiol conjugates, 92% of the ether-soluble radioactivity cochromatographed with estradiol, and 3.8% cochromatographed with estrone. Estrogen-sulfurylating activity was localized in the cytosol of subcellular fractions of RL95-2 cells. The sulfoconjugation of estrogens by RL95-2 cells may prove useful as a model for the investigation of estrogen metabolism in endometrial carcinoma cells.
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PMID:Estrogen sulfoconjugation by human endometrial cancer cells (RL95-2) in culture. 669 41

The ability of human endometrium to synthesize estrogen from testosterone (T) was investigated. Normal and malignant endometrial specimens were incubated in a complete nutrient medium with 1 muC/ml (approximately 10 pmol/ml) of [3H]T for 20 hrs. Various estrogens: estrone (E1), estradiol (E2), estrone sulfate (E1S), and estradiol-3-sulfate (E2S) were isolated from cultured tissue and medium. The capacity of aromatization, expressed in pmol of estrogen formed/g of tissue, of proliferative endometria was found to be significantly higher than that of secretory endometria (prol. n=12, 0.53 +/- 0.21, vs sec. n=13, 0.15 +/- 0.09, mean +/- s.d., P less than 0.005). In nine cancer endometrial specimens studied, the estrogen produced varied from 0.3 to 15 pmol/g of tissue. These studies represent the first evidence that human endometrium is capable of synthesizing estrogens from delta 4 androgens at a concentration similar to plasma level. The changes of the capacity of aromatization during the two phases of the menstrual cycle indicate that the estrogen synthesis in endometrium is apparently regulated by hormones. The presence of aromatase in cancer endometria may play an important role in promoting the cell growth in estrogen sensitive endometrial cancer.
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PMID:Estrogen synthesis in normal and malignant human endometrium. 711 84

The study included 191 patients with obesity, atherosclerosis, diabetes mellitus, endometrial cancer, breast cancer and healthy subjects of various age. Somatomedin activity was determined by incorporation of radioactive natrium sulfate in vitro into the cartilage of female rats. The results of the study showed that somatomedin activity was not changed in subjects with normal metabolic parameters and ranged from 0.47 to 0.69 U/ml. In patients with diabetes mellitus, atherosclerosis and obesity accompanied by increased blood concentration of cholesterol and triglycerides, somatomedin activity rose up to 1.36- 1.62 U/ml. In patients with breast and endometrial cancer somatomedin activity was also increased, particularly in those with hypercholesterolemia and hypertriglyceridemia (3.04 U/ml for breast cancer patients and 2.20 U/ml for endometrial cancer patients). Theoretically, this may promote proliferation of somatic cells and thus contribute to tumor processes in oncological patients whose pool of cells is extremely sensitive to mitogenic agents.
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PMID:Interrelation between lipidemia and somatomedin activity in cancer and age-associated pathology. 713 38

Various aspects of climacteric treatment with natural human estrogens are discussed. Estradiol, estradiol valerate, estron sulfate, or estriol are used separately or together in various preparations to treat the symptoms of approaching menopause. Estrogen treatment causes proliferation of the endometrium and causes a decrease in LHRH, FSH, and LH secretion. Treatment can take the form of continuous or cyclic treatment with estrogens alone, or sequential estrogne/gestagen preparations can be used. Ovarian function decreases as menopause approaches and results in the cessation of ovulation. Then the hypolutein phase begins, during which the secretion of progesterone is reduced and menstrual bleeding irregularities begin to occur. Eventually, estrogen production decreases so much that menstruation ceases completely, and symptoms such as heat flashes are experienced. Women who want treatment for climacteric symptoms but who want no regular menstrual bleeding can be administered low doses of pure estrogen. Regular abrasio control of endometrial development should be performed, however. Pure estrogen treatment can also be used in the case of hysterectomized women. Otherwise, a sequential treatment is generally indicated. Possible side effects of estrogen substitution therapy are changes in the genitalia, breasts, menstrual bleeding, blood pressure, and weight. There is also an indication that estrogen use can induce endometrial cancer. Besides the definite contraindication of endometrial cancer, relative contraindications of estrogen therapy include breast cancer, reduced liver function, thromboembolic disease, and serious hypertension. Estrogen therapy is to be used to solve acute climacteric symptoms; women should be well informed about possible side effects and that the therapy is no panacea for all menopausal problems.
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PMID:[Peroral treatment with natural human estrogens in the climacteric]. 744 54

I read with interest Dixit's review article concerning the liver and (OC) oral contraceptives (Can J Surg 23:222, 1980), and I think attention should be drawn to 1 or 2 possibly erroneous generalizations and inaccuracies. The author refers to both OCs and menopausal replacement medications and lists a group of general long-term effects which he describes as being common. In fact their rate of occurrence is quite low. Endometrial carcinoma has been reported to be associated with estrone sulfate therapy but not with combined estrogen-progesterone OCs; however, Silverberg and Makowski reported several cases of endometrial carcinoma associated with the use of the sequential OC Oracon, a product containing dimethisterone. Sequential agents are no longer used and indeed it is possible that combination agents may have a protective effect vis-a-vis endometrial carcinoma. Further, it is confusing to state that estrogen may be causally associated with carcinoma of the cervix; this was not the intent of the quoted article. All currently used OCs contain 19-nortestosterones but substituted progesterones have been used in the past. The progestins that have been used are numerous but should include norithisterone and d-norgestrel, the latter being 1 of the most widely used synthetic progestins. Estrogens are currently used in doses as low as 0.02 mg, and 0.035 mg doses are usual. The plasma coagulation proteins are indeed elevated (page 225) but in addition to those mentioned, factors 5 and 8 should have been included. In the section on changes in pregnancy (page 226), "increased serum fibrinogen" is mentioned. Surely the author means "plasma fibrinogen," as serum is totally devoid of that particular protein. This very comprehensive review emphasizes the effect of these potent agents on hepatic function in general. In view of the elevation of coagulation protein levels produced by OCs (and the consequent tendency to hypercoagulability), it might be interesting to ask general surgeons how frequently they discontinue OC medication before they perform elective surgery.
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PMID:Effects of oral contraceptives on the liver. 744 54


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