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Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 15, 2004; 10(2): 292-294
Published online Jan 15, 2004. doi: 10.3748/wjg.v10.i2.292
Expression of COX-2 proteins in gastric mucosal lesions
Lian-Zhen Yu, Heng-Jun Gao, Jian-Feng Bai, Gu Sun, Han-Lin Zhao, Liang Sun, Kun Miu, Zhi-Quan Zhao
Lian-Zhen Yu, Heng-Jun Gao, Liang Sun, Kun Miu, Zhi-Quan Zhao, Department of Gastroenterology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China
Jian-Feng Bai, Gu Sun, Han-Lin Zhao, Department of General Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China
Author contributions: All authors contributed equally to the work.
Supported by the Natural Science Fund of the Educational Committee of Jiangsu Province, No.125FA9608 and Fund of Nanjing Medical University for Outstanding Young Faculty
Correspondence to: Heng-Jun Gao, Department of Gastroenterology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China
Received: April 2, 2003
Revised: May 10, 2003
Accepted: May 17, 2003
Published online: January 15, 2004
Abstract

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 cancer and the relationship between COX-2 expression and H pylori 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 by rapid urea test combined with pathological stating/14C urea breath test.

RESULTS: The positive rate and staining intensity of mutant COX-2 gene expression in gastric cancer were significantly higher than those in paracancerous tissues (66.7% vs 26.7%) (P < 0.01, P < 0.001). There was a significant 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 than that with negative H pylori (50.6% vs 18.1%, 60.0% vs 33.3%) (P < 0.05).

CONCLUSION: COX-2 overexpression was found in a large proportion of gastric cancer tissues compared with matched non-cancerous tissues and was significantly associated with advanced tumor stage and lymph node metastasis. Overexpression of COX-2 plays an important role in tumor progression of gastric cancer. COX-2 may also play a role in the early development/promotion of gastric carcinoma and is associated with H pylori infection.

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