Gastric Cancer
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 15, 2003; 9(2): 246-249
Published online Feb 15, 2003. doi: 10.3748/wjg.v9.i2.246
Association of cyclooxygenase-2 expression with Hp-cagA infection in gastric cancer
Xiao-Lin Guo, Li-Er Wang, Shu-Yan Du, Chen-Ling Fan, Li Li, Peng Wang, Yuan Yuan
Xiao-Lin Guo, Yuan Yuan, Cancer Institute, The First Hospital, China Medical University. Shenyang, 110001, Liaoning Province, China
Shu-Yan Du, Chen-Ling Fan, Li-Er Wang, Li Li, Peng Wang, Center Laboratory, The First Hospital, China Medical University. Shenyang, 110001, Liaoning Province, China
Author contributions: All authors contributed equally to the work.
Supported by The National Basic Research Program (973) of China, No. G1998051203
Correspondence to: Dr. Yuan Yuan, Cancer institute, the First Hospital, China Medical University, Shenyang, 110001, Liaoning Province, China. yyuan@mail.cmu.edu.cn
Telephone: +86-24-23256666-6153
Received: April 18, 2002
Revised: May 4, 2002
Accepted: June 11, 2002
Published online: February 15, 2003
Abstract

AIM: To observe the expression of cyclooxygenase-2 (COX-2) and to investigate the association between COX-2 expression and infection with cytotoxic-associated gene A (cagA) positive strain Helicobacter pylori (Hp) in human gastric cancer, and subsequently to provide fresh ideas for the early prevention of gastric cancer.

METHODS: 32 Specimens of gastric cancer and corresponding adjacent normal gastric mucosa were obtained from patients who had undergone surgical operations of gastric cancer. All the samples including 1 case of stomach malignant lymphoma and 31 cases of gastric adenocarcinoma were confirmed by pathology diagnosis. The expression of COX-2 in 32 specimens of gastric cancer and corresponding adjacent normal gastric mucosa was quantitatively determined and analyzed with Flow Cytometry, and the levels of COX-2 protein were compared between specimens with cagA+Hp infection and those without cagA+Hp infection. The cagA gene in 32 specimens of gastric cancer was detected by polymerase chain reaction (PCR) method.

RESULTS: Twenty-seven of 32 (84%) specimens of gastric cancer showed over-expression of COX-2, compared with the adjacent normal gastric mucosa. cagA+ gene were detected from 19 specimens of gastric cancer, but not from the other 13 specimens. The levels of COX-2 protein in 19 specimens of gastric cancer with cagA+Hp infection (the number of positive cells was 73.82 ± 18.2) were significantly higher than those in the 13 specimens without cagA+Hp infection (the number of positive cells was 35.92 ± 22.1).

CONCLUSION: COX-2 is overexpressed in gastric cancer and cagA+Hp infection could up-regulate the expression of COX-2 in gastric cancer in human. There may also exist another way or channel to regulate the expression of COX-2 in gastric cancer in addition to cagA+Hp infection. Therefore, applying COX-2 selective inhibitors could be an effective and promising way to prevent gastric cancer.

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