Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The progression of neoplasms is frequently associated with thromboembolic complications. Coagulation proteins, particularly tissue factor (TF), have been shown to play a role in tumor growth and metastatic dissemination. TFPI is the principal inhibitor of TF-dependent pathway of blood coagulation, but previous studies failed to detect antigenic TFPI in cancer tissue. Recently, a second inhibitor of tissue factor dependent pathway, TFPI-2 (also known as placental protein 5 [PP5] or matrix-associated serine protease inhibitor [MSPI]), has been described. Information on the presence of TFPI-2 within the malignant tumor tissue still remains obscure, and thus the aim of this study was to evaluate the expression of TFPI-2 in loco in several different neoplasms. TFPI-2 expression was demonstrated by immunohistochemical procedures in neoplastic cells of laryngeal, breast, gastric, colon, pancreatic, renal and endometrial cancer, as well as glial neoplasms. The intensity of staining was not uniform, with higher intensity in more differentiated tumors. G3 breast, gastric, endometrial and colon cancer cells revealed populations of cells that were either TFPI-2 positive or negative. Gastric and renal cancer tissue exhibited the presence of TFPI-2 in tumor infiltrating macrophages. TFPI-2 was also observed in normal tissue of the breast, stomach, colon and pancreas. These data demonstrate that the expression of TFPI-2 diminishes with an increasing degree of malignancy, which may suggest a role for TFPI-2 in the maintenance of tumor stability and inhibition of the growth of neoplasms.
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PMID:Immunohistochemical localization of tissue factor pathway inhibitor-2 in human tumor tissue. 1287 37

Estrogen and progestin combination in hormone replacement therapy (HRT) increases the incidence of breast cancer, but decreases the endometrial cancer risk of unopposed estrogen. Therefore, a SERM such as Tibolone, that delivers the beneficial, but not the adverse side effects, of steroid hormones would be clinically advantageous. However, data from the Million Women Study suggests that Tibolone increases the risk of both breast and endometrial cancer. Herein, we assessed the estrogenic and progestagenic actions of Tibolone using transvaginal sonography studies and an in vitro model of breast (ZR-75, MCF7) and endometrial cancer (Ishikawa). The known cancer associated proteins (ER, EGFR, STATS, tissue factor and Bcl-xL) were selected for study. Transvaginal sonography demonstrated that postmenopausal women treated with Tibolone displayed a thinner endometrium than in the late proliferative phase, but had a phenotype characteristic of the secretory phase, thus demonstrating the estrogenic and progestagenic actions of this SERM. In vitro, Tibolone acted as an estrogen in downregulating ER and upregulating Bcl-xL, yet as progesterone, increasing STAT5 and tissue factor in breast cancer cells. The increase in tissue factor by Tibolone correlated with its coagulative potential. Interestingly, EGFR was up-regulated by progesterone in the breast and by estrogen in endometrial cells, while Tibolone increased protein levels in both cell types. In conclusion, this study further demonstrates the estrogenic and progestagenic nature of Tibolone. The pattern of regulation of known oncogenes in cells of breast and endometrial origin dictates caution and vigilance in the prescription of Tibolone and subsequent patient monitoring.
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PMID:In vivo and in vitro estrogenic and progestagenic actions of Tibolone. 1623 3

Despite numerous endometrial cancer cell lines, little is know about the progression and transition of primary cultured endometrial tumours. Herein, a stage I grade III endometrial adenocarcinoma was maintained in primary culture and the phenotypic and protein expression changes were observed in relation to passage number. At early passage numbers, cultured human endometrial cancer (CHEC) cells displayed classic epithelial cell morphology, growing in groups in a glandular structure and staining positive for cytokeratin. However, with increasing passage number, CHEC cells changed in morphology to display a stromal phenotype which was accompanied by a significant reduction in cytokeratin and increases in alpha-actin and vimentin expression. Simultaneous culture of stromal cells isolated from the original tumour failed to show the same morphological characteristics or protein expression patterns. We further characterised CHEC cells through a screening of cancer related proteins, among others, caveolin-1 and Tissue factor in comparison with established cancer cell lines and corresponding non-cancerous cells. This report demonstrates that endometrial adenocarcinoma cells in culture can undergo phenotypic and protein expression changes reminiscent of epithelial-mesenchymal transition. This work suggests that primary tumours and cell lines displaying stromal morphologies may have undergone epithelial-mesenchymal transition from an adenocarcinoma origin.
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PMID:Characterization and phenotypic variation with passage number of cultured human endometrial adenocarcinoma cells. 1803 81