Reactive Oxygen Species Analysis in Gastritis Patients and P53 Methylation Analysis in Gastric Tumor Cell Line Ags Infected by Helicobacter Pylori
Epidemiological studies in humans and animal models support the idea that Helicobacter pylori a gram-negative spiral bacterium, first described by Warren and Marshall in 1983, is one of the risk factors for the induction of gastric cancer. H. pylori infection is the cause of chronic gastritis, peptic ulcer disease, gastric mucosa associated lymphoid tissue lymphoma and cancer of the distal stomach (1). Virulent or less virulent H. pylori strains can be determined by the presence or absence of cag pathogenicity island (PM) genes including the cagA gene and vacA genotypes. The expression of different genes of the cag PAI (total of 26 genes) seems to be essential for virulence. CagA and VacA proteins are highly antigenic (2). H. pylori strains expressing CagA show increased synthesis of chemokines, promote neutrophil infiltration in the gastric epithelium and stimulate synthesis of interleukin-8 (3). In the repetitive regions of the cag 7 gene within the cag PAI of H. pylori deletions and insertions are detected representing a target for mutations (4). In addition, Covacci et al (5) have suggested that new different quasi-species of H. pylori strains which possess or loose their cag PAI are generated during chronic infection by H. pylori.
KeywordsHPLC Filtration Lymphoma Codon EDTA
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