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AIM:To investigate the expression of COX-2 proteins ingastric mucosal lesions and to assess the relationshipbetween COX-2 expression and type,pathologic stage,differentiation,or lymph node metastasis in gastric cancerand the relationship between COX-2 expression and Hpyloriinfection in gastric mucosal lesions.METHODS:Thirty patients with gastric carcinomaunderwent surgical resection.Samples were taken fromtumor site and paracancerous tissues,and ABCimmunohistochemical staining was used to detect theexpression of COX-2 proteins.H pylori was determined byrapid urea test combined with pathological stating/~(14)C ureabreath test.RESULTS:The positive rate and staining intensity of mutantCOX-2 gene expression in gastric cancer were significantlyhigher than those in paracancerous tissues (66.7% vs 26.7%)(P<0.01,P<0.001).There was a significant correlation betweenCOX-2 and pathologic stage or lymph node metastasis typeof gastric carcinoma (76.0% vs 20.0%,79.2% vs 16.7%)(P<0.05).No correlation was found between COX-2expression and type or grade of differentiation (P>0.05).COX-2 expression of intestinal metaplasia (IM) or dysplasia(DYS) with positive H pylori was significantly higher thanthat with negative H pylori(50.6% vs 18.1%,60.0% vs33.3%) (P<0.05).CONCLUSION:COX-2 overexpression was found in a largeproportion of gastric cancer tissues compared with matchednon-cancerous tissues and was significantly associated withadvanced tumor stage and lymph node metastasis.Overexpression of COX-2 plays an important role in tumorprogression of gastric cancer.COX-2 may also play a role inthe early development/promotion of gastric carcinoma andis associated with H pylori infection.
AIM: To investigate the expression of COX-2 proteins in gastric mucosal lesions and to assess the relationship between COX-2 expression and type, pathologic stage, differentiation, or lymph node metastasis in gastric cancerand the relationship between COX-2 expression and Hpylori infection in gastric mucosal lesions. METHODS: Thirty patients with gastric carcinoma underwent surgical resection. Samples were taken from tumor site and paracancerous tissues, and ABC immunohistochemical staining was used to detect the expression of COX-2 proteins. H pylori was determined byrapid urea test combined with pathological stating / ~ (14 ) C ureabreath test .RESULTS: The positive rate and staining intensity of mutant COX-2 gene expression in gastric cancer were significantlyhigher than those in paracancerous tissues (66.7% vs 26.7%) (P <0.01, P <0.001) correlation between COX-2 and pathologic stage or lymph node metastasis type of gastric carcinoma (76.0% vs 20.0%, 79.2% vs 16.7%) (P <0.05) .No correlation was found between COX-2 expression and type or grade of differentiation (P> 0.05) .COX-2 expression of intestinal metaplasia (IM) or dysplasia (DYS) with positive H pylori was significantly higher thanthat with negative H pylori (50.6% vs 18.1 %, 60.0% vs33.3%) (P <0.05) .CONCLUSION: COX-2 overexpression was found in a largeproportion of gastric cancer tissues compared with matched non-cancerous tissues and was significantly associated withadvanced tumor stage and lymph node metastasis. Overexpression of COX-2 plays an important role in tumorprogression of gastric cancer. COX-2 may also play a role inthe early development / promotion of gastric carcinoma and associated with H pylori infection.