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

The histochemical method was used for determining glycogen, phosphorylase, glycogensynthetase, and glucose-6-phosphatase in order to evaluate the effect of progesterone on different morphological forms of cancer of the endometrium in man. On the basis of histochemical analysis of changes in the carbohydrate metabolism in 29 cases of cancer before and after treatment with progesterone a conclusion is drawn that sensitivity of tumours of the endometrium to hormonotherapy only partially depends upon the degree of their morphological differentiation.
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PMID:[A histochemical study of the effect of progesterone on the carbohydrate metabolism enzymes of different morphologic forms of endometrial cancer]. 17 78

Studies on glycogen metabolism in tissues of endometrial cancer with various morphological structure have indicated that in most cases irrespective of the level of differentiation endometrial tumors contain no glycogen and show a slight activity of glycogensynthetase, phosphorylase and oxido-reductive enzymes. However, among the tumors under study there may be cases, which are characterized by a high content of glycogen and enzymes related with its metabolism. In these patients endometrial cancer was preceded by persistant disorders in the menstrual cycle. The relation between two types of the glycogen metabolism in endometrial cancer and the state of endogenous hormonal background is discussed.
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PMID:[Glycogen level in endometrial cancer]. 126 18

The glycogen content and glycogen synthetase and glycogen phosphorylase levels were studied in tissues of endometrial carcinoma obtained from 30 patients (27 postmenopausal and three premenopausal) before and after administration of progestogen, and the values were compared with those obtained previously from normal endometrial tissue of premenopausal patients. After the patients had undergone an oral glucose tolerance test (OGTT), the progestogen Lyndiol (lynestrenol, 5.0 mg, and mestranol, 0.15 mg) was administered daily for seven days. In 15 cases of well differentiated carcinoma the glycogen content after the progestogen administration, accompanied by a corresponding increase in the glycogen synthetase enzyme levels, was significantly higher (P less than 0.005) than that in the initial tissue, whereas in the other 15 cases of less differentiated carcinoma no change was observed. This finding that hormonal stimulus in well differentiated carcinoma leads to a similar effect on glycogen metabolism as in normal endometrium of the proliferative phase of the menstrual cycle, supports the possibility of progestogen therapy for human endometrial cancer.
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PMID:Hormone dependency of carcinoma of the human endometrium. Effect of progesterone on glycogen metabolism in the carcinoma tissue. 621 87

To elucidate potential mechanisms involved in the increased incidence of endometrial carcinomas in tamoxifen-treated patients, we examined the in-vitro effects of tamoxifen on endometrial cancer cells. The effects of tamoxifen, alone and in combination with oestradiol, on cell proliferation, plasminogen activator (PA) activity, glycogen synthase and phosphorylase activities, p53 protein concentration, and collagenase expression were assessed in two human adenocarcinoma cell lines. These lines were the oestrogen receptor-positive (Ishikawa) cells, representing a well-differentiated endometrial adenocarcinoma, and oestrogen receptor-negative (HEC-1A) cells, derived from a poorly differentiated endometrial adenocarcinoma. Tamoxifen or oestradiol alone and their combination significantly enhanced cellular proliferation of Ishikawa but not of HEC-1A cells. Both lines produced appreciable PA activity, most of which was of the urokinase type. Tamoxifen and oestradiol stimulated this activity in Ishikawa cells but not in HEC-1A cells. The effect of oestradiol was dose-dependent in a linear fashion, while tamoxifen produced a stimulation peaking at 10(-8) M and declining at higher concentrations. Tamoxifen in combination with oestradiol exhibited a synergistic effect on proliferation and on PA activity. The response of PA extended beyond the increase in proliferation, leading to higher specific activity of PA in the tamoxifen-treated cultures. In Ishikawa cells, oestradiol also increased glycogen synthase and glycogen phosphorylase activities, while tamoxifen markedly suppressed these enzymes. Oestradiol, tamoxifen, and their combination had no apparent effect on the expression of protein p53 in Ishikawa cells, or on gelatinase activity in either Ishikawa or HEC-1A cells. The present findings imply that tamoxifen produces oestrogen-agonistic effects on cell proliferation and PA activity, and oestrogen antagonistic effects on glycogen synthase and glycogen phosphorylase activities, but fails to regulate p53 and gelatinase expression. The tamoxifen-responsive systems were only observed in oestrogen-responsive adenocarcinoma cells. Thus, only certain potential oncogenic effects of tamoxifen can be simulated in vitro, and when present, these effects are enhanced in the presence of oestradiol.
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PMID:Tamoxifen exerts oestrogen-agonistic effects on proliferation and plasminogen activation, but not on gelatinase activity, glycogen metabolism and p53 protein expression, in cultures of oestrogen-responsive human endometrial adenocarcinoma cells. 946 46

A gene (MTAP) that encodes the enzyme 5'-deoxy-5'-methylthioadenosine (MTA) phosphorylase has been identified on chromosome 9p21 and cloned. The substrate of this enzyme, MTA, inhibits aminopropyltransferases that synthesize polyamines from putrescine and decarboxylated S-adenosylmethionine. This enzyme normally cleaves MTA to adenine and 5'-methylthioribose-1-phosphate, which are recycled to adenine nucleotides and methionine, respectively. Cancers with deletions of the MTAP gene may be especially susceptible to chemotherapeutic regimes which interfere with purine or methionine utilization. The purpose of this study was to determine deletion of the MTAP gene in endometrial cancer using a polymerase chain reaction-based method. Therefore, 50 endometrial adenocarcinomas were studied. Partial or total deletions of the MTAP gene were detected in 7 (14%) of these cancers. There were no significant relationships between gene deletion and patient age, pathological grade or clinical stage (p > 0.05). The findings indicate that deletion of the MTAP gene does occur in a subgroup of endometrial cancer. The present work may be extended to the development of molecular diagnosis of MTAP gene deletion in other cancers and assist in selecting appropriate chemotherapy.
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PMID:MTAP gene deletion in endometrial cancer. 962 96