Interaction between Helicobacter pylori and host genetic variants in gastric carcinogenesis

Helicobacter pylori (H. pylori) is the definite carcinogen of gastric cancer. H. pylori infection induces chronic inflammation, causes DNA damage and aberrant methylation of genes and these pathways are involved in H. pylori-related gastric carcinogenesis. Polymorphisms of the genes involved in thes...

Full description

Saved in:
Bibliographic Details
Published in:Future oncology (London, England) England), 2016-09, Vol.12 (18), p.2127-2134
Main Authors: Jia, Zhi-Fang, Zhang, Song-Ling, Cao, Xue-Yuan, Zhou, Bao-Sen, Jiang, Jing
Format: Article
Language:English
Subjects:
Atrophy
Biomarkers
Carcinogenesis
Cytokines
Deoxyribonucleic acid
Disease Susceptibility
DNA
DNA Methylation
DNA Repair
Gastric cancer
Gene Expression Regulation, Neoplastic
Genes
Genetic Variation
Helicobacter Infections - complications
Helicobacter Infections - microbiology
Helicobacter pylori
Host-Pathogen Interactions
Humans
Infections
Inflammation
Inflammation - complications
Inflammation - genetics
Inflammation - metabolism
Polymorphism
Polymorphism, Genetic
Population
Stomach Neoplasms - etiology
Stomach Neoplasms - metabolism
Studies
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Helicobacter pylori (H. pylori) is the definite carcinogen of gastric cancer. H. pylori infection induces chronic inflammation, causes DNA damage and aberrant methylation of genes and these pathways are involved in H. pylori-related gastric carcinogenesis. Polymorphisms of the genes involved in these pathways could alter susceptibility to gastric cancer. In this mini review, we focused on the role of polymorphisms in these genes on the susceptibility to gastric cancer, with a particular emphasis on their possible interactions with H. pylori infection. We found that many studies on this theme did not simultaneously report H. pylori infection and the interactions remained inconclusive.
ISSN:1479-6694
1744-8301
DOI:10.2217/fon-2016-0233