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

Certain epidemiologic, histologic, and biochemical data on the effects of estrogens and progestogens on the endometrial, physical, psychological, and lipid status of postmenopausal women are reviewed. Unopposed estrogen replacement increases the risk of endometrial cancer not only while treatment is being taken but also for many years after it is discontinued. Strategies must be developed for posttreatment surveillance. The addition of a cyclic progestogen reduces this risk, but it is not clear whether the reduction is to, or below, that observed in an untreated population. Protective doses of C-19 (norethindrone) and C-21 (medroxy-progesterone acetate) progestogens are suggested. All progestogens may cause physical, psychological, and metabolic side effects. In addition, most women taking cyclic progestogens experience regular withdrawal bleeding. Continuous/combined therapy has been introduced to minimize these side effects and induce amenorrhea. Published data on the efficacy and safety of continuous combined therapy are few. Although the regimen is effective in relieving menopausal symptoms and inducing endometrial atrophy in most patients, side effects of progestogen are common and there is a high incidence of bleeding in the first few months, which is unacceptable to many patients. In our view, the effect of continuous combined therapy on lipids and lipoproteins has not been properly addressed. Based upon the available literature, we believe that the enthusiasm for continuous combined therapy is premature and we urge caution in its use until further, more conclusive, data become available.
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PMID:The role and use of progestogens. 217 92

The use of megestrol acetate in treatment of malignancy (endometrial carcinoma, ovarian cancer, prostate cancer, breast cancer, renal cell carcinoma, malignant melanoma), endometrial hyperplasia, benign prostatic hypertrophy, contraception, anorexia, cachexia and weight loss is reviewed, concluding with a toxicity profile. Megestrol acetate was introduced in 1971 for treatment of endometrial carcinoma. Megestrol acetate is probably effective in proportion to the number of cytoplasmic progesterone receptors, but it has not been tested in a Phase III trial. For ovarian cancer it has been reported to be effective in 1 trail at doses of 800 mg/day. Prostate cancer, although difficult to assess, responds to megestrol acetate at doses of 120 mg/day because of its suppression of gonadotropins, its inhibition of 5alpha-reductase and its binding to the dihydrotestosterone receptor. Megestrol acetate permits a lower dose of diethylstilbestrol, and thus lower toxicity. There is apparently a dose-response between megestrol acetate and breast cancer, along with a response dependent on the number and type of estrogen and progestin receptors. Responses are better in postmenopausal women, and additive with other agents such as tamoxifen and mitomycin C. The medium duration of effect is 6-8 months. It has no effect on renal cancer or malignant melanoma. Megestrol acetate can be considered as an effective medical alternative to surgery for endometrial hyperplasia or benign prostatic hypertrophy. As a contraceptive in inhibits sperm transport rather than ovulation, but also causes irregular bleeding. Megestrol acetate has few side effects, and has the advantage of stimulating appetite and weight gain, a benefit in cancer patients.
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PMID:Megestrol acetate: clinical experience. 247 90

More than 30% of the colony formation of dispersed tumor cells was inhibited by medroxyprogesterone acetate (MPA) in 2 out of 6 cases of endometrial cancer, in 1 out of 6 cases of cervical cancer, and in 3 out of 12 cases of ovarian cancer. The colony formation inhibited by MPA was not related to clinical stage or histological type. There was no significant difference in the tumor angiogenesis factor (TAF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. TAF activity was inhibited by MPA in 4 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 9 out of 12 cases of ovarian cancer. There was no significant difference in the fibroblast growth factor (FGF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. FGF activity was inhibited by MPA in 3 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 10 out of 12 cases of ovarian cancer. The cases in which the colony formation was inhibited by MPA were not related to the cases in which TAF or FGF activity was inhibited by MPA. Therefore, MPA may reduce neovascularization induced by TAF and FGF, and can depress secondary spreading of some endometrial, cervical and ovarian cancer via the mechanism of terminal process of secondary spreading, regardless of the presence of glucocorticoid actions similar to that of cortisol, and the reduction of cell proliferation.
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PMID:Inhibition of tumor angiogenesis activity by medroxyprogesterone acetate in gynecologic malignant tumors. 247 53

In 31 women with haemorrhage during the climacteric and postmenopausal period the authors investigated as risk factors of endometrial carcinoma glandular cystic hyperplasia during the perimenopause and signs of oestrogenization of the endometrium in the postmenopausal period. Based on the results of anamnestic data, gynaecological, laboratory and histological examination treatment, incl. administration of gestagens, was outlined. None of the patients who had medroxyprogesterone acetate treatment had a relapse of dysfunctional bleeding or endometrial carcinoma during the one year follow up period. The authors present the results of control examinations after six months treatment. They give an outline of centralized care of risk groups of women in a centre for the pathology. This is a methodological paper, endometrial the basis for a subsequent investigation on the subjects.
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PMID:[Initial experience with centralized care of women with bleeding in the climacteric and postmenopausal period]. 252 73

We examined the effect of medroxyprogesterone acetate (MPA) on secondary spreading of endometrial cancer. There was no significant difference in the adhering capacity of dispersed Ishikawa cells (derived from well-differentiated endometrial cancer) to a cell basement membrane matrix, fibronectin or laminin between cells treated with MPA, with cortisol, and without treatment. The adhering capacity of cells treated with cortisol to collagen type IV was higher than that without treatment. However, the adhering capacity was little affected by treatment with MPA. These results indicate that although cortisol may induce the initial process of metastasis by inducing the attachment of tumor cells to the basement membrane of vascular endothelium, MPA has no influence on the attachment, although it has a glucocorticoid action similar to that of cortisol. There was no significant difference in tumor angiogenesis factor (TAF) or fibroblast growth factor (FGF) activity of the tumor extract from Ishikawa cell colonies between cortisol-treated and control group. TAF or FGF activity of the MPA-treated group was lower than that of the control group. MPA may reduce the neovascularization in the terminal process of metastasis via the reduction of TAF and FGF produced by tumor cells, in spite of its glucocorticoid action.
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PMID:Effect of medroxyprogesterone acetate on secondary spreading of endometrial cancer. 252 39

Estrogen biosynthesis (aromatase activity) was investigated in human adenomyosis tissue and compared with that of the normal myometrium, endometrium, and endometrial cancer tissues. Homogenates were incubated with [1,2,6,7-3H]androstenedione and NADPH at 37 degrees C for 1 h. After stopping the enzymatic reaction with ethyl acetate, [4-14C]estrone and [4-14C]estradiol-17 beta were added to the incubated sample. Estrone and estradiol were purified and identified by Bio-Rad AG1-X2 column chromatography, thin-layer chromatography and co-crystallization. Estrogen formed in the incubated sample was calculated from the 3H/14C ratio of the final crystal. The value for estrone formed from androstenedione was 52-132 fmol.h-1.g-1 wet weight. Aromatase activity in the adenomyosis tissues was higher than that in normal endometrial or myometrial tissues, but lower than that found in myometrial or endometrial tumour tissue. Furthermore, we investigated the effect of danazol, progesterone, and medroxyprogesterone acetate on adenomyosis cells in primary cultures. Aromatase activity in adenomyosis was blocked by danazol, but stimulated by progesterone and MPA. These results indicate that aromatase activity in adenomyosis may contribute to the growth of the ectopic endometrial tissue which occurs in this disease.
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PMID:Estrogen biosynthesis in human uterine adenomyosis. 252 61

Progesterone receptors (PR) were measured in 18 cases of endometrial carcinoma using the dextran-coated charcoal assay. The histological changes and PR levels of the endometrial carcinoma after the medroxyprogesterone acetate (MPA) treatment were studied. A higher PR levels were observed in well-differentiated tumors. After treatment with MPA, the PR content was reduced and histological appearance similar to normal endometrium was noticed. The histological changes of the tumor was closely related to the receptor levels.
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PMID:[Progesterone receptors in endometrial carcinoma and their response to medroxyprogesterone acetate]. 253 67

The colony-formation of Ishikawa cells, which originate from well differentiated endometrial cancer, and produce progestogen receptors (PR), was inhibited by high concentrations of medroxyprogesterone acetate (MPA). However, the colony-formation was not inhibited by norethindrone (ENT), as a luteohormone or 17 beta-hydroxy-11 beta-(4-dimethylaminophenyl-1)-17 alpha(prop-1-ynyl)-estra-4, 9-dien-3-one (RU-486), as an antiprogestogen. Colony-formation in cells treated with MPA alone was not significantly different from that in those treated with MPA combined with either ENT or RU-486. ENT and RU-486 have high affinity with PR as does MPA. If the suppressive effect by MPA on colony-formation is mediated via PR, then this suppression should be competitively inhibited by ENT or RU-486. Our findings indicate that the effect of MPA is not mediated via PR.
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PMID:Mechanism of antitumoral activity of medroxyprogesterone acetate for endometrial cancer. 253 82

Proliferation and differentiation of the normal endometrium are orderly regulated by female sex steroid hormones. In this connection, development and growth of endometrial cancer have also thought to be controlled in part by sex steroid hormones. Furthermore, some of the sex steroid hormones, progesterone, for example, are used as therapeutic agents in the management of endometrial cancer. The role of estrogen as a promotion factor of endometrial cancer is understood by unopposed estrogen hypothesis, and relative excess of estrogen unopposed by gestagen is regarded as an important factor for the development of endometrial cancer. High dose administration of gestagen has been used as a therapeutic agent of endometrial cancer over these three decades, and now the oral administration of medroxyprogesterone acetate (MPA) is mainstay, with response rate of approximately 30%. However, recently some cases with serious side effect, mainly thrombosis, have been reported. These cases should be regarded as a grave warning to easy usage of MPA. Therefore, the search for more effective and safe way for clinical application have to be requested; for example, clarification of the precise mechanism of anti-tumor effect of MPA on endometrial cancer or development of new hormonal therapeutic agents. Moreover, basic research in the field of cancer and hormone may create a new era in cancer therapy in the future.
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PMID:[Growth of endometrial cancer and hormone]. 253 93

Correlations were identified between tumor morphobiochemical characteristics and basic parameters of reproductive homeostasis in 256 cases of endometrial carcinoma. A correlation was established between the levels of cytoplasmic receptors to estradiol (ER) and progesterone (PR), on the one hand, and morphological differentiation and spontaneous secretion in tumor tissue, on the other. A direct correlation was found between ER and metastatic spread to regional lymph nodes, and no correlation--between ER and PR and major parameters of reproductive homeostasis. A significant decrease in ER, PR, gonadotropins, estradiol and colpocytological reaction indexes followed hormone therapy with hydroxyprogesterone capronate and medroxyprogesterone acetate. The criteria of endometrial carcinoma patients sensitivity to progestin therapy were as follows: ER and PR levels--more than 30.0 fmol/mg protein, estradiol--more than 30-50 pg/ml and colpocytological index--over 40%.
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PMID:[Effect of progestin therapy on the level of cytoplasmic receptors in patients with cancer of the corpus uteri]. 254 46


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