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Helicobacter pylori infection and gastric carcinoma:Not all the strains and patients are alike

World Journal of Gastrointestinal Oncology 2016年第1期8卷 40-54页

作者： natale figura luigi marano elena moretti antonio ponzetto department of medical surgical and neurological sciencesuniversity of siena and policlinico s.maria alle scotte53100 SienaItaly general minimally invasive and robotic surgerydepartment of surgeryhospital san matteo degli infermi06049 SpoletoPerugiaItaly department of molecular and developmental medicine university of siena53100 SienaItaly department of medical sciences university of torino10126 TorinoItaly

Gastric carcinoma(GC) develops in only 1%-3% of Helicobacter pylori(H. pylori) infected people. The role in GC formation of the bacterial genotypes, gene polymorphisms and host's factors may therefore be important. The risk of GC is enhanced when individuals are infected by strains expressing the oncoprotein CagA, in particular if CagA has a high number of repeats containing the EPIYA sequence in its C'-terminal variable region or particular amino acid sequences flank the EPIYA motifs. H. pylori infection triggers an inflammatory response characterised by an increased secretion of some chemokines by immunocytes and colonised gastric epithelial cells; these molecules are especially constituted by proteins composing the interleukin-1beta(IL-1β) group and tumour necrosis factor-alpha(TNF-α). Polymorphisms in the promoter regions of genes encoding these molecules, could account for high concentrations of IL-1β and TNF-α in the gastric mucosa, which may cause hypochlorhydria and eventually GC. Inconsistent results have been attained with other haplotypes of inflammatory and anti-inflammatory cytokines. Genomic mechanisms of GC development are mainly based on chromosomal or microsatellite instability(MSI) and deregulation of signalling transduction pathways. H. pylori infection may induce DNA instability and breaks of double-strand DNA in gastric mucocytes. Different H. pylori strains seem to differently increase the risk of cancer development run by the host. Certain H. pylori genotypes(such as the cagA positive) induce high degrees of chronic inflammation and determine an increase of mutagenesis rate, oxidative-stress, mismatch repair mechanisms, down-regulation of base excision and genetic instability, as well as generation of reactive oxygen species that modulate apoptosis; these phenomena may end to trigger or concur to GC development.

关键词： Helicobacter pylori infection CagA cagagene polymorphism Haplotype Human gene mutation Genemethylation Gastriccarcinoma Inflammatorycytokine

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