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)

Maspin, a mammary serine protease inhibitor, was originally reported as a tumor suppressor gene in breast cancer. The purpose of the present study was to examine maspin expression and evaluate its clinicopathological significance in endometrial cancer. We examined maspin expression immunohistochemically in 41 cases with endometrioid adenocarcinoma. DNA methylation status at the maspin promoter region was determined by the methylation-specific polymerase chain reaction method. Aberrant maspin expression was observed in 27 (66%) of 41 endometrioid adenocarcinomas but not in normal endometrial glands. Maspin immunoreactivity of the tumor cells varied in incidence and density among tumors. Positive staining was correlated significantly with the presence of squamous differentiation (presence vs absence = 11/11 [100%] vs 16/30 [53%], P < 0.05), and nuclear subcellular localization of maspin protein was also significantly associated with squamous differentiation (nuclear positive vs nuclear negative = 6/11 [54%] vs 2/30 [6.7%], P < 0.05). An inverse correlation between their immunoreactivity and methylation status was observed (P < 0.01). Three of the four cell lines established from endometrioid adenocarcinomas overexpressed maspin mRNA and its protein product. In a maspin-negative cell line, maspin expression was induced by treatment with 5-aza-2'-deoxycytidine, a DNA demethylating agent. There was no significant correlation between maspin expression and any clinicopathlogical data. These findings suggest that maspin induced by DNA demethylation at the promoter region may contribute to squamous differentiation of tumor cells in endometrioid adenocarcinomas.
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PMID:Aberrant maspin expression in human endometrial cancer. 1682 96

Maspin is a member of the serpin family, whose expression is altered in neoplasia and malignancies of many tissues. Underexpression of maspin has been reported in breast and prostatic cancers, but in some cancers such as ovarian, colorectal and pancreatic carcinoma, it was found to be up-regulated. This study aimed at demonstrating the expression of maspin in human endometrial tissue and searching for any altered expression in endometrioid adenocarcinoma of the endometrium compared to normal endometrium. The expression level of the maspin gene was studied using reverse transcriptase-polymerase chain reaction (RT-PCR) performed on RNA extracted from 34 endometrial cancer samples (including 24 with FIGO stage I disease and 10 with FIGO stage III disease) and 28 normal endometrium in proliferative or secretory phases. Immunohistochemical staining was also performed on 10 cases of endometrial cancer (6 FIGO stage I cases and 4 FIGO stage III cases) as well as 15 normal endometrium. Semi-quantitative RT-PCR revealed that the expression of maspin was significantly up-regulated in both stage I (p<0.01) and stage III (p<0.01) endometrial cancer compared with normal endometrium. However, no significant difference in maspin expression was demonstrated between stage I and stage III endometrial cancer. Immunostaining of all tissue sections revealed an immunopositive signal in the nuclei of the normal or cancerous endometrial glandular cells. In 60% of the cancer cases, cytoplasmic staining was also evident. Our results suggested that there is up-regulated expression of maspin in endometrioid endometrial adenocarcinoma. Cytoplasmic immuno-expression of maspin is common in endometrial cancer. It may play a role in the malignant transformation of human endometrial tissue.
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PMID:Expression of maspin in endometrioid adenocarcinoma of endometrium. 1720 79

Dominant negative (DN) mutations of tumor suppressor p53 (TP53) are clinically associated with cancer progression and metastasis of endometrial malignancy. To investigate the DN effect on tumor migration and invasion, we generated cells that stably co-expressed wild-type (wt) and R273H DN mutant TP53 (273H cells), and wt and R213Q recessive mutant TP53 (213Q cells), by transfection in endometrial cancer cells HHUA that expressed wt p53. R273H, but not R213Q, repressed wt p53-stimulated transcription of p21, Bax, and MDM2. 273H cells also showed markedly increased in vitro invasion and migration potentials, and displayed reduced Maspin, PAI-1, and KAI1 mRNA expressions as compared with 213Q and wt cells. The induction of wt p53 function by use of Adriamycin resulted in the inhibition of the invasion/migration capacity in association with the up-regulation of p53 target genes to a far greater degree in 213Q and wt cells than in 273H cells. R273H expression in p53-null cancer cell SK-OV-3 and Saos-2 did not significantly affect cell invasion and migration activities. Taken together, these results suggest that transdominance of R273H mutant over wt p53 rather than a gain-of-function promotes tumor metastasis by increasing invasion and migration in HHUA cells.
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PMID:p53 dominant-negative mutant R273H promotes invasion and migration of human endometrial cancer HHUA cells. 1763 7