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

The responsiveness and action mechanisms of steroid hormones and epidermal growth factor on human endometrial carcinoma cells are analyzed by using in vitro culture system. 1) The Ishikawa cells, derived from a well differentiated endometrial adenocarcinoma and possess ER and PR, are shown to respond to estrogens by increasing a variety of parameters, viz cell proliferation, PR levels, ALP and DNA polymerase activities. 2) ER and PR of those cells are localized in the nuclei by immunocytochemical staining using the monoclonal antibodies against to ER and PR, confirming the correctness of Gorski and Greene's one step theory involving the action mechanisms of steroid hormones. 3) Progestins reduced the ER level and stimulate E2DH activities and glycogen content, which are completely abolished by anti-progestin (RU486), suggesting that PR of those cells should be functional. 4) These responses to steroid hormones of Ishikawa cells are synergistically enhanced or appeared earlier by addition of EGF. 5) The main metabolite of E2 incubated with Ishikawa cells is E2-3-sulfate instead of E1, indicate that the higher estrogenic status may be persisted in endometrial cancer tissues.
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PMID:[Responsiveness and mechanisms of action of steroid hormones in human endometrial adenocarcinoma cells]. 251 14

The mechanism of action of sex steroid hormones on endometrial carcinoma was analyzed by a cell culture system. 1) Estrogenic actions such as enhancement of ALP activity, PR level and cellular growth were confirmed in Ishikawa endometrial carcinoma cells which possess ER. 2) ER and PR are both localized immunocytochemically in the nuclei of Ishikawa cells, confirming the correctness of Gorsky and Greene's theory in endometrial carcinoma. 3) In Ishikawa cells with PR, progestins stimulated E2DH activity and glycogen synthesis and reduced ER level, thus proving the existence of their hormonal action. We cannot, however, rule out the pharmaceutical action of progestin, because a decrease in nucleic acid syntheses and ALP activity, alteration in electron microscopic observation and finally cellular death were observed in endometrial cancer cells without PR. 4) Conversely, Tamoxifen, anti-estrogen, stimulated the cellular growth in serum-free environment of culture. We must therefore be careful in using it clinically.
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PMID:[Mechanism of action of endocrine therapy of endometrial carcinoma]. 273 78

Heat-stable ALP has been attracting attention as one of the oncodevelopmental proteins. ALP are now subdivided by biochemical methods into three major groups e.g. tissue-unspecific, intestinal and term placental isoenzymes. Furthermore, term placental ALP in cancer is classified into L-leucine insensitive-Regan and L-leucine sensitive-Nagao isoenzymes. In this paper, we report ALP isoenzyme profiles of normal endometrium and endometrial cancers. 21 cases of normal endometrium and 11 cases of endometrial cancer were examined, and the ALP activity of their butanol extracts was measured by Fishman's method. To identify the ALP isoenzyme pattern, biochemical methods such as 65 degrees C heat-treatment and amino acid inhibition tests were carried out. Most of the ALP in both normal endometrium and endometrial cancers showed biochemical characteristics of tissue-unspecific ALP isoenzyme. A very small amount of term placental isoenzyme was found in normal endometrium. In endometrial cancers, term placental isoenzyme was often found at a higher level than in normal endometrium. Nagao isoenzyme was also found to emerge in a few endometrial cancer cases. From these data it was suggested that the ALP isoenzyme of endometrium underwent a change and "enzyme deviation" occurred during the course of endometrial carcinogenesis and that the ALP isoenzyme deviation might have occurred due to a change in ALP isoenzyme gene expression accompanying cancerous change.
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PMID:[Biochemical studies on alkaline phosphatase isoenzyme profile in endometrial cancer]. 620 74

Estrogen replacement therapy is commonly used to replace the loss of estrogen in post-menopausal women. However, it is not suitable to be used in women taking tamoxifen as both of the drugs increase the risk of endometrial cancer. This project aimed to study the potential of using the natural compound glabridin in combination with tamoxifen as a drug for estrogen replacement therapy. Ishikawa and MCF-7 cells were used to investigate the estrogenic activities stimulated by the combination of tamoxifen and glabridin through ALP and MTT assays. The expressions of the ESR1 and bcl-2 genes have also been determined using RT-PCR. The results indicated that the combination of 1 x 10(-5)M tamoxifen and 1 x 10(-6)M glabridin exhibited estrogenic activities and suppressed cell growth in both cell lines. The relative expressions of ESR1 and bcl-2 genes indicated that the estrogenicity expressed by the combinatory drug was regulated by estrogen receptor a; however, the reduction in cell proliferation was not modulated by bcl-2 anti-apoptotic proteins. These results suggested that the combination of tamoxifen and glabridin has potential to be used as an estrogen replacement drug with a reduced risk of endometrial cancer that has arisen from the intake of tamoxifen.
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PMID:The Combinatory Effects of Glabridin and Tamoxifen on Ishikawa and MCF-7 Cell Lines. 2659 62