Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AIM:To study the telomerase expression in gastric carcinoma and its clinical implications.METHODS:Telomerase activity was examined in gastric cancer and corresponding normal tissues using a modified TRAP (telomeric repeat amplify-cation protocol) assay (TRAP-eze) in tissue samples from 94 gastric carcinomas and 58 normal tissues, 12 gastric adenomas and 9 gastric ulcer lesions.RESULTS:Telomerase activity was present in 81 of the 94 (86.2%) gastric cancer tissues, whereas no telomerase activity was detected in any normal tissues.The incidence of telomerase activity in gastric cancer tissues was unrelated to the tumor diameter, histological grade, tumor invasion in depth, lymph node metastasis and TNM stage.CONCLUSION:Telomerase plays an important role in carcinogenesis and progression of gastric cancer, and it is suggested to be a useful tumor marker.
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PMID:Telomerase activity in gastric cancer and its clinical implications. 1181 56

Epithelial dysplasia is considered the only one true histological marker of gastric cancer. In the present study we have evaluated the real clinical importance of epithelial dysplasia divided into low-grade (70 patients, mean age 59.2 years) and high-grade (50 patients, mean age 58 years) dysplasia. Furthermore, it has been made a comparison with the corresponding endoscopic picture and an evaluation of the real meaning of p53 positivity. The clinical outcome subdivision of epithelial dysplasia was effected according to the criteria of Rugge: association with or progression to gastric cancer, persistence or regression. The endoscopic patterns have been divided into ulcerous lesions and non-ulcerous lesions. The immunohistochemical study has been carried out with the utilization of a p53 antibody (Dako, Glostrup, Denmark). From the analysis of the data it comes out that low-grade dysplasia is associated with or progressed to gastric cancer in a low percentage of cases (about 8.5%), while high-grade dysplasia is associated with or progressed to gastric cancer in a high percentage of cases (about 74%), by this proving itself to be a real histological marker of gastric cancer. The cases of epithelial dysplasia associated with or progressed to gastric cancer are significantly associated with an endoscopic picture of gastric ulcer (ulcer-cancer). Nonetheless, the cases of epithelial dysplasia in correspondence of non-ulcerous lesions have been noticed to be associated with or progressed to advanced gastric cancer. The evaluation of p53 did not positively correlate with the clinical progression of the epithelial dysplasia and with TNM classification in case of gastric cancer. Therefore, the evaluation of p53 does not represent a useful marker in the clinical practice.
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PMID:[High and low grade gastric epithelial dysplasia: clinical management, endoscopic assessment of p53]. 1497 11

RKIP is proposed as a new metastasis suppressor. Our recent study showed that RKIP inhibits malignant phenotypes of gastric cancer cells. However, the underlying mechanism of RKIP function in gastric cancer is unclear. This study aimed to investigate the correlation of RKIP, STAT3 and cyclin D1 expression in the tumorigenesis of gastric cancer. RKIP, STAT3 and cyclin D1 proteins were detected by immunohistochemistry in tissues of gastric ulcer (n = 27), gastric adenomatous polyp (n = 7), intestinal metaplasia (n = 26), dysplasia (n = 40), gastric carcinoma (n = 169) and metastatic lymph node (n = 36). RKIP, STAT3 and cyclin D1 mRNA levels were analyzed by RT-PCR in SGC7901 cells. We found that RKIP protein expression was significantly decreased in advanced gastric cancer and metastatic lymph node tissues while cyclin D1 and STAT3 protein expression was markedly increased in severe dysplasia, gastric cancer and metastatic lymph node tissue (P < 0.01). RKIP expression in gastric cancer was negatively correlated with the invasion, TNM stage and lymphoid node metastasis (P < 0.01), while cyclin D1 and STAT3 expression was positively correlated with histological differentiation and lymphoid node metastasis (P < 0.01). RKIP protein level was negatively correlated with cyclin D1 and STAT3 protein level, while cyclin D1 protein level was positively correlated with STAT3 protein level in gastric cancer samples. Moreover, reconstitution of RKIP in SGC7901 gastric cancer cells led to reduced cyclin D1 and STAT3 mRNA levels. In conclusion, these data suggest that RKIP inhibits gastric cancer metastasis via the downregulation of its downstream target genes STAT3 and cyclin D1.
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PMID:Correlation of RKIP, STAT3 and cyclin D1 expression in pathogenesis of gastric cancer. 2533 33