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 tumor suppressor gene p16, located on chromosome 9p21, encodes the cell cycle regulatory protein, p16. Inactivation of the p16 gene could lead to uncontrolled cell growth. It was examined that methylation of the p16 gene 5'CpG island of the tumor suppressor gene may be an important mechanism for transcriptional inactivation. In order to determine the role of methylation status of the 5'CpG island and abnormal expression of incarcinogenesis of endometrial carcinoma (EC), Methylation-Specific PCR (MSP) was used to determine the methylation status of p16 gene 5'CpG islands of 62 cases of EC. Loss or decrease of p16 expression was analyzed by immunohistochemistry (IHC) and homozygous deletion of exon1 (E1) and exon2 (E2) was determined by complex PCR. Ten specimens of normal tissues and adjacent tissues of tumor displayed no methylation and showed normal expression of p16. In E1 and E2 of the 62 EC, we found that 24.2% (15/62) were methylated, 54.8% (33/62) lost or reduced p16 expression, 16.1% (10/62) and 30.6% (19/62) had deletions of E1 and E2 respectively. There were 9.68% (6/62) and 46.6% (29/62) deletions of both or either of E1 and E2 respectively. Inactivation of p16 gene is a frequent event and positively correlated with pathological grades and clinical stages in EC. p16 gene methylation was an important event in the development of EC. MSP is an accurate and relatively simple method for evaluating the methylation status of a related gene.
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PMID:[Significance of methylation and abnormal expression of p16 gene in endometrial carcinoma]. 1547 4

Cables is a novel cell cycle regulatory protein that interacts with cdk2, cdk3, and cdk5. Cables inhibits cdk2 activity by enhancing cdk2 tyrosine 15 phosphorylation by Wee1, which consequently leads to inhibition of cell growth. Loss of Cables expression was found in many human cancers, especially colon and endometrial cancer. However, the role of the Cables gene in cancer development remains unclear. This study was undertaken to analyze transcripts of Cables gene in endometrial and colon cancers. The analysis of RT-PCR products of the Cables gene revealed shortened products in each sample along with the product of the expected size. Sequence analysis indicated that these shortened products represented eight intragenic deletions in Cables mRNA transcripts. Analysis of DNA from the same tumor sample failed to show genomic rearrangements corresponding to the transcripts containing deletions, suggesting that the deletions are the result of RNA splicing. Sequence analysis demonstrated that five of the deletions resulted from alternative splicing (splicing at the exon/intron boundary consensus sites), whereas the remaining three deletions resulted from aberrant splicing (splicing at sites not considered to be exon/intron boundary sites). All three aberrant splicing products were only detected in tumor tissues. Ectopic expression of one of the aberrant splicing products, which was detected in both endometrial and colon carcinomas, resulted in increased cell growth rate in human colon carcinoma HT-29 cells, suggesting a role as a dominant negative mutant.
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PMID:Aberrant splicing of cables gene, a CDK regulator, in human cancers. 1617 68

Cyclin A, a cell cycle regulatory protein, promotes cell proliferation and has been observed to be highly expressed in cancer and to promote tumor growth; however, its value as a marker for endometrial carcinoma has not yet been established. Accordingly, the aim of the present study was to clarify whether cyclin A can be used as a cell proliferation marker using the endometrial carcinoma cell lines Ishikawa and HEC-50B, derived from patients with low-grade and high-grade cancer, respectively. The expression of cyclin A was determined by flow cytometry using double staining with FITC and 7-AAD, and immunocytochemical staining. The results were compared to those of Ki-67, the widely used cell proliferation marker that is considered to be a prognostic marker in endometrial cancer. The flow cytometry results revealed that cyclin A expression was significantly higher in HEC-50B than in Ishikawa cells during the logarithmic growth phase. In addition, cyclin A expression was consistently higher than Ki-67 expression in the examined cell lines. Immunocytochemical staining confirmed cyclin A expression in HEC-50B and Ishikawa cells, demonstrating significantly higher expression during the logarithmic growth phase than during the stationary phase. By contrast, Ki-67 was expressed in almost 90% of the cells, irrespective of their growth state. These results indicate that cyclin A expression is significantly increased in cells with higher proliferative ability and is specifically expressed in cells that have passed the G1-S checkpoint. Therefore, cyclin A may be a reliable proliferation biomarker for endometrioid carcinoma.
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PMID:Cyclin A is a reliable proliferation marker in endometrial cancer cell lines. 3098 14