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

Recent reports have suggested that the presence of progesterone receptor correlates with other well known predictors of a favorable outcome for endometrial cancer patients. To test this hypothesis, we reviewed the records of 154 patients who had undergone a hysterectomy for adenocarcinoma of the endometrium, and pelvic irradiation if poor prognostic factors were present. The 3 year disease-free survival for all clinical Stage I patients was 80%. Patients with progesterone receptor levels greater than or equal to 100 had a 3 year disease-free survival of 93% compared with only a 36% 3 year disease-free survival for patients with progesterone receptor less than 100 (p less than .0001, log rank test). To determine whether elevated progesterone receptor was an independent prognostic factor for disease-free survival in endometrial cancer, or just correlated with the other well-known predictors, bivariate and multivariate analyses were conducted. Our results indicate the progesterone receptor levels are the single most important prognostic indicator of 3 year disease-free survival in clinical Stage I endometrial cancer, with only cervical involvement and peritoneal cytology being significant prognostic variables after adjusting for progesterone receptor levels.
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PMID:The predictive value of progesterone receptor levels in endometrial cancer. 274 95

A direct correlation between steroid hormone receptor level, tumor differentiation and pathogenetic pattern of tumor was established in 49 patients with endometrial carcinoma. Dynamics of tamoxifen-induced changes in progesterone receptor level proved an important criterion of hormone dependence of endometrial tumor.
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PMID:[Effect of tamoxifen on the content of cytoplasmic steroid hormone receptors of the tumor in patients with cancer of the corpus uteri]. 275 79

Samples of 40 endometrial carcinomas were examined by immunohistochemical methods for CA19-9, CA125 and CEA. CA19-9 was detected in 93%, CA125 in 65% and CEA in 58%. CA19-9 was detected in more than 50% of tumor cells in 14 cases and the same was true for CA125 in six cases. In no tumor was CEA found in more than half the cells. The distribution of CA125 and CEA was markedly more heterogenous than that of CA19-9. There was no statistically significant correlation between immunohistochemical markers on the one hand, and estrogen and progesterone receptor content on the other. A correlation between histological grading and marker detection was only found for CA19-9. CA19-9 was detected in almost all endometrial carcinoma samples, and was the most homogenously distributed. This makes CA19-9 a possibly useful tumor marker for endometrial carcinoma.
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PMID:CA19-9, CA125 and CEA in endometrial carcinoma tissue and its relation to hormone receptor content and histological grading. 285 10

Creatine kinase (CK), isocitrate (ICDH) and glucose-6-phosphate dehydrogenase (G-6-PD) activities and cytosol oestrogen (REc) and progestin (RPc) receptors have been measured in twenty post-menopausal subjects with endometrial carcinoma. Diagnostic curettage and hysterectomy specimens were obtained from each patient with intervening medroxyprogesterone acetate therapy (MPA). In RPc rich tumours the activity of creatine kinase was significantly increased following MPA and was attributed to an increase in the BB-isoform. There was a similar though less significant increase in ICDH activity. Neither CK nor ICDH were significantly increased following MPA therapy in progesterone receptor poor specimens. There was a small but significant increase in G-6-PD activity following MPA regardless of RPc content. REc was decreased in some but not all RPc rich tumours following MPA and the trend was significant. The highly significant increase in CK activity confirms the apparent response of this enzyme to progesterone in normal human endometrium during the menstrual cycle.
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PMID:The effects of medroxyprogesterone acetate on enzyme activities in human endometrial carcinoma. 293 31

Alkaline phosphatase activity in human endometrial cancer cells of the estrogen-responsive Ishikawa line was markedly stimulated (3-20-fold in 4 days) by estrogens, 5 alpha-dihydrotestosterone, and dehydroepiandrosterone but not by testosterone, medroxyprogesterone acetate, glucocorticoids, several peptide hormones, prostaglandins, or growth factors. Maximum responses to estradiol were obtained at concentrations between 10(-9) and 10(-7) M; at 10(-8) M estradiol, the highest activity was reached 48-72 h after addition of the hormone. A linear relationship between enzyme activity at 48 h and the length of exposure to the hormone was observed. Dibutyryl cyclic guanosine 3':5'-monophosphate, but not dibutyryl cyclic adenosine 3':5'-monophosphate enhanced alkaline phosphatase activity and acted synergistically with estradiol. trans-4-Monohydroxytamoxifen completely antagonized the stimulatory effect of estradiol and had no agonistic activity. Dihydrotestosterone and dehydroepiandrosterone appear to exert their effects, at least in part, by interacting with estrogen receptors, since the simultaneous presence in the medium of monohydroxytamoxifen abolished their influence on alkaline phosphatase activity. The specific antiandrogen monohydroxyflutamide partially antagonized the effect of these hormones, suggesting that their action involved androgenic mechanisms as well. Exposure to elevated temperature and to specific inhibitors identified alkaline phosphatase of Ishikawa cells as a placental-type isoenzyme, thus contrasting with the nonplacental type found in glandular epithelial cells of normal endometrium and in another human endometrial cancer cell line, HEC-50. This study extends our previous observations of estrogen responsiveness in the Ishikawa cell line. In addition to the previously reported stimulatory effects on growth and progesterone receptor levels, we are now describing the stimulation by estrogens and C19 steroids of an enzyme, alkaline phosphatase, which can be used as a convenient end point to examine mechanisms of hormonal action.
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PMID:Effects of steroid hormones and antisteroids on alkaline phosphatase activity in human endometrial cancer cells (Ishikawa line). 293 30

The effects of estradiol on DNA polymerase alpha activity were investigated in an estrogen-responsive human endometrial cancer cell line (Ishikawa) derived from a well differentiated endometrial adenocarcinoma. These cells are known to respond to estradiol by increasing progesterone receptor levels, alkaline phosphatase activity, and cell density. Four- to 5-fold increases in DNA polymerase alpha activity occurred when estradiol was added to cultures of Ishikawa cells in medium containing charcoal-treated fetal bovine serum. Maximal stimulation was achieved at 18 h during incubations with 10(-8) M estradiol, but significant effects also were found with 10(-9) and 10(-6) M. These effects were almost completely counteracted by a 100-fold excess of 4-hydroxytamoxifen. At 10(-6) M, the antiestrogen had no influence on the basal levels of DNA polymerase alpha. Medroxyprogesterone acetate (10(-6) M) was ineffective as either an enhancer of enzymatic activity or an antiestrogen when tested in combination with 10(-8) M estradiol, even in the presence of appreciable levels of specific progesterone binders. The responsiveness of the Ishikawa cells to estrogen contrasts with the lack of effects of estradiol on DNA polymerase alpha activity in another human endometrial adenocarcinoma cell line (HEC-50).
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PMID:Effects of estradiol on deoxyribonucleic acid polymerase alpha activity in the Ishikawa human endometrial adenocarcinoma cell line. 294 47

The anti-tumor activities of steroid compounds on endometrical cancer (Ishikawa cell line) were examined in vitro by human tumor clonogenic assay (HT CA). Clinically effective progestational compounds including medroxyprogesterone acetate (MAP), and 17 alpha hydroxy-progesterone caproate were effective. Norethindrone (ENT), which is also a potent progestational compound, and RU486, which is known to be a progesterone antagonist were ineffective in this in vitro system, neither having any influence on the effect of MAP. These results indicated that the anti-tumor activity of MAP did not proceed via the so-called progesterone receptor system. Morphological changes induced by MAP in undifferentiated endometrial cancer, the effectiveness of tamoxifen, hormonochemotherapy, and the use of MAP for adjuvant therapy and prophylaxis were also discussed.
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PMID:[Hormone dependency and progestogen therapy in the treatment of endometrial cancer]. 295 4

A nude mouse system where the biological, morphological and biochemical characteristics of human endometrial carcinoma are maintained during serial transplantation has been previously described. Applications of this system to the study of (a) hormonal sensitivity (b) treatment strategies and (c) progesterone receptor physiology of human endometrial carcinomas are presented here.
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PMID:Nude mouse system in the study of tumor biology, treatment strategies and progesterone receptor physiology in human endometrial carcinoma. 296 35

The use of medroxyprogesterone acetate (MPA) in therapy of patients with endometrial cancer has been recently examined by the Japan Gynecological Cancer Treatment Group. The response rate of oral MPA was 23.6% (13/55 evaluables) and the average period up to the onset of response was 15.2 weeks (4-28 wks). The response rate was higher in well-differentiated tumors than in poorly differentiated ones. Although it is well known that steroid hormone action is mediated by steroid hormone receptor, the presence of progesterone receptor in cancer tissue seems to be not absolutely necessary for the responsibility to MPA, a potent progestational compound. The reason was studied, in vitro, in our laboratory by using the technique of human tumor clonogenic assay. In this system, MPA showed a marked suppressive effect on the colony formation of endometrial cancer cells. Similar effects were also observed with progesterone, 17 alpha-hydroxyprogesterone caproate and megestrol acetate. Norethindrone and norgestrel, which are both potent progestational compounds, showed almost no anticancer activity on Ishikawa cell in this in vitro system. It became clear that progestational activity was not always associated with anticancer activity, and norethindrone had no influence on the inhibitory effect of MPA, although norethindrone has a strong affinity for progesterone receptor. Similarly, RU 486, which is known as a potent antiprogestogen agent and has a high affinity to progesterone receptor, did not influence the effect of MPA. These results clearly indicated that the anticancer activity of MPA was not mediated by high affinity low capacity progesterone receptor, and a pharmacological effect must be considered for understanding the effect of MPA on endometrial cancer.
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PMID:[Progestogen therapy in the treatment of endometrial cancer--clinical results and mechanism of steroid action]. 296 80

Forty-six eligible women with metastatic endometrial cancer were randomly allocated to receive monthly cycles of either CAF (cyclophosphamide, adriamycin, 5-fluorouracil) or CAF plus Provera 200 mg daily for 3 weeks followed cyclically by Tamoxifen 20 mg daily for 3 weeks. Overall response rates of 15 and 43% were seen with CAF and CAF plus hormonal therapy. Using a multivariate analysis of the results, this difference is significant (P value 0.05). In 8 patients with operable endometrial cancer, negative estrogen receptor concentration (ER less than 15 fmole/mg protein) and Grade 3 disease, the clinical course was aggressive in 4 patients with systemic and local relapse. In 10 other similar patients (negative ER and Grade 3) who received adjuvant cyclical hormonal therapy only 1 relapsed and the other 9 are disease-free for an average of more than 31 months. Sequential cyclical hormonal therapy with ER and progesterone receptor analysis has a place in the management of endometrial carcinoma.
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PMID:Efficacy of sequential cyclical hormonal therapy in endometrial cancer and its correlation with steroid hormone receptor status. 297 97


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