Literature DB >> 14966904

Expression of nuclear factor-kappa B and target genes in gastric precancerous lesions and adenocarcinoma: association with Helicobactor pylori cagA (+) infection.

Gui-Fang Yang1, Chang-Sheng Deng, Yong-Yan Xiong, Ling-Ling Gong, Bi-Cheng Wang, Jun Luo.   

Abstract

AIM: To examine the expression of nuclear factor kappaB (NF-kappaB) 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-kappaB/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-kappaB/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-kappaB in IM III, and DYSII-III. A significantly higher expression level of NF-kappaB/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-kappaB/p65 activated by H pylori cagA. Inhibiting the activity of NF-kappaB is an effective and promising way to prevent intestinal type gastric carcinoma.

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Year:  2004        PMID: 14966904      PMCID: PMC4716967          DOI: 10.3748/wjg.v10.i4.491

Source DB:  PubMed          Journal:  World J Gastroenterol        ISSN: 1007-9327            Impact factor:   5.742


  61 in total

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6.  Influence of Helicobacter pylori on reactive oxygen-induced gastric epithelial cell injury.

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9.  Role of Helicobacter pylori CagA+ strains and risk of adenocarcinoma of the stomach and esophagus.

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  21 in total

1.  The impact of C-MYC gene expression on gastric cancer cell.

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2.  Association between cyclin D1 polymorphism with CpG island promoter methylation status of tumor suppressor genes in gastric cancer.

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Review 5.  Helicobacter pylori infection and gastric cancer: host, bug, environment, or all three?

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6.  The influence of TXNDC5 gene on gastric cancer cell.

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Review 7.  Nuclear factor kappa B role in inflammation associated gastrointestinal malignancies.

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Review 8.  MYC and gastric adenocarcinoma carcinogenesis.

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Review 9.  Causal role of Helicobacter pylori infection in gastric cancer: an Asian enigma.

Authors:  Kartar Singh; Uday C Ghoshal
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Review 10.  Perspectives on new biomarkers in gastric cancer: diagnostic and prognostic applications.

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Journal:  World J Gastroenterol       Date:  2014-09-07       Impact factor: 5.742

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