Abstract
ObjectiveCOX‐2 is frequently expressed in gastric cancer, which may play a active role in carcinogenesis, tumor invasion and metastatis. To evaluate the distribution and expression of COX‐2 in various stages of gastric carcinogenesis and monitor the changes of COX‐2 in intestinal metaplasia (IM) after H. pylori eradication.MethodsGastric biopsies were selected from a group of H. pylori infected patients with various histological diagnosis of chronic active gastritis (CAG, n=40), gastric atrophy (GA, n=20), IM (n=51) and adenocarcinoma (CA, n=25). Non‐infected (n=40) were included as control. Expression of COX‐2 was examined by immunohistochemistry and scored in a semiquantitative manner: 0 = negative , 1 = <5% cells with positive staining, 2 = 5‐30%, 3 = 30‐60% and 4 = >60%. Cellular localization of COX‐2 was further confirmed by in‐situ hybridization of COX‐2 mRNA using an anti‐sense RNA probe. In subgroup of patients with IM, the experissions of COX‐2 one‐year after successful H. Pylori eradication was compared with pre‐treatment level.ResultsCOX‐2 expressions were detected in all H.Pylori‐infected patients irrespective of histological diagnosis. In Contrast, only 14 (35%) H. Pylori‐negative control expressed weak COX‐2 expression (median score 0 vs 2; P<0.0001). However, there was no difference in the intensity of COX‐2 expression between CAG, GA, IM and CA patients. Among the 17 IM patients who had received successful H. Pylori eradication therapy, there was a modest reduction of COX‐2 expressions in both epithelial (P=0.049) and stromal cells (P=0.001) at one‐year. However, there was no significant change in the severity of IM, not any correlation between changes in IM and COX‐2 expression, at one‐year follow‐up.ConclusionBoth premalignant and malignant gastric lesions show strong COX‐2 expression. Although successful eradication of H. pylori reduces the level of COX‐2 expression, there is no association with regression of IM at one year.
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