BACKGROUND: The cag pathogenicity island (PAI), a Helicobacter pylori virulence factor, is associated with the pathogenesis of gastric cancer. Matrix metalloproteinase-7(MMP-7) is upregulated in the epithelial cells of gastric cancer. To date, there is limited information available on the role of cag PAI and MMP-7 in precursor lesions. In this study, we aimed to identify virulent H. pylori strains and the expression of MMP-7 in samples of gastric epithelial dysplasia and intramucosal cancer. METHODS: One hundred and twelve tissues excised by endoscopic mucosal resection, 76 specimens with gastric epithelial dysplasia and 36 with intramucosal cancer, were examined. All tissue samples were paired with surrounding normal epithelial tissue samples. We performed polymerase chain reaction for cagA and cagL in neoplasia and paired normal specimens, and assessed the matrix metalloproteinase (MMP)-7 expression by immunohistochemical staining. RESULTS: There was a significant difference in the frequencies of cagA or cagL between specimens with gastric dysplasia and those with intramucosal cancer. We confirmed greater expression of MMP-7 immunoreactivity in intramucosal cancers infected with a virulent H. pylori strain. CONCLUSION: Our results suggest that infection with a virulent H. pylori strain was associated with early-stage gastric cancer and that carcinogenesis was associated with cag PAI-dependent MMP-7 upregulation.
BACKGROUND: The cag pathogenicity island (PAI), a Helicobacter pylori virulence factor, is associated with the pathogenesis of gastric cancer. Matrix metalloproteinase-7(MMP-7) is upregulated in the epithelial cells of gastric cancer. To date, there is limited information available on the role of cag PAI and MMP-7 in precursor lesions. In this study, we aimed to identify virulent H. pylori strains and the expression of MMP-7 in samples of gastric epithelial dysplasia and intramucosal cancer. METHODS: One hundred and twelve tissues excised by endoscopic mucosal resection, 76 specimens with gastric epithelial dysplasia and 36 with intramucosal cancer, were examined. All tissue samples were paired with surrounding normal epithelial tissue samples. We performed polymerase chain reaction for cagA and cagL in neoplasia and paired normal specimens, and assessed the matrix metalloproteinase (MMP)-7 expression by immunohistochemical staining. RESULTS: There was a significant difference in the frequencies of cagA or cagL between specimens with gastric dysplasia and those with intramucosal cancer. We confirmed greater expression of MMP-7 immunoreactivity in intramucosal cancers infected with a virulent H. pylori strain. CONCLUSION: Our results suggest that infection with a virulent H. pylori strain was associated with early-stage gastric cancer and that carcinogenesis was associated with cag PAI-dependent MMP-7 upregulation.
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