Gastric Cancer
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 15, 2004; 10(4): 491-496
Published online Feb 15, 2004. doi: 10.3748/wjg.v10.i4.491
Expression of nuclear factor-kappa B and target genes in gastric precancerous lesions and adenocarcinoma: Association with Helicobactor pylori cagA (+) infection
Gui-Fang Yang, Chang-Sheng Deng, Yong-Yan Xiong, Ling-Ling Gong, Bi-Cheng Wang, Jun Luo
Gui-Fang Yang, Yong-Yan Xiong, Ling-Ling Gong, Bi-Cheng Wang, Jun Luo, Department of Pathology, Zhongnan Hospital, Wuhan University, Wuhan 430071, Hubei Province, China
Chang-Sheng Deng, Department of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan 430071, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Supported by grants from the Bureau of Science and Technology of Hubei Province, No. 2003AA301C27
Correspondence to: Dr. Gui-FangYang, Department of Pathology, Zhongnan Hospital, Wuhan University, Wuhan 430071, Hubei Province, China. caiyang@public.wh.hb.cn
Telephone: +86-27-67813159
Received: June 5, 2003
Revised: July 8, 2003
Accepted: July 24, 2003
Published online: February 15, 2004
Abstract

AIM: To examine the expression of nuclear factor kappaB (NF-κB) and its target genes in intestinal metaplasia (IM), dysplasia (DYS) and gastric carcinoma (GC) infected with Helicobacter pylori (H pylori) and to investigate the mechanism underlying H pylori cytotoxin associated gene A (cag A) infection leading to gastric adenocarcinoma.

METHODS: Expressions of NF-κB/p65 and its target genes: c-myc, cyclinD1 and bcl-xl were immunohistochemically examined in 289 cases of gastric biopsy and resection specimens from patients with IM, DYS and GC infected with H pylori. H pylori in the above mentioned tissues was detected by Warthin-Starry stain and rapid urease tests. IgG antibody to cagA in sera of the patients was measured by ELISA.

RESULTS: The positive rates of NF-κB/p65 were significantly higher in groups with cagA of IMI-II(28/33), IM III(48/52), DYSI(27/31), DYS II-III(28/32), GC(35/40) than in groups without cagA of IMI-II(4/17), IMIII(3/20), DYSI(3/20), DYSII-III(6/21), GC(10/23). The expressions of c-myc, cyclinD1, and bcl-xl were significantly higher in groups with cagA of IM III(47/52, 49/52, 46/52), DYSII-III(29/32, 26/32, 25/32) than in groups without cagA of IM III(8/20, 7/20, 5/20), DYSII-III(10/21, 8/21, 3/21), which were in conformity with the expression of NF-κB in IM III, and DYSII-III. A significantly higher expression level of NF-κB/p65, c-myc, cyclinD1 and bcl-xl was detected in intestinal type GC(27/28, 18/28, 22/28, 24/28) than in diffuse type GC(8/12, 3/12, 3/12, 6/12), respectively.

CONCLUSION: There may be two different molecular mechanisms in the occurrence of intestinal and diffuse type gastric carcinomas. Intestinal type gastric carcinoma is strongly associated with high expression of c-myc, cyclinD1 and bcl-xl through NF-κB/p65 activated by H pylori cagA. Inhibiting the activity of NF-κB is an effective and promising way to prevent intestinal type gastric carcinoma.

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