Interaction Between Helicobacter Pylori and Host Genetic Variants in Gastric Carcinogenesis

Abstract

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.

miR-7 Increases Cisplatin Sensitivity of Gastric Cancer Cells Through Suppressing mTOR

“…3 Previous studies have shown that the tumorigenesis of GC is involved in both genetic and epigenetic alterations, including the activation of oncogenes and/or the suppression of tumor suppressor genes. [4][5][6] Mounting evidence suggests that noncoding microRNAs (miRNAs) play key roles in the development of GC. MicroRNAs s are a large class of endogenous noncoding RNAs, 21-23 nucleotides in length, that regulate about 30% of human gene expression.…”

Silencing of immunoglobulin superfamily containing leucine-rich repeat inhibits gastric cancer cell growth and metastasis by regulating epithelial–mesenchymal transition

“…GC is usually diagnosed at advanced stage, and recurrence and metastasis are the greatest challenges in the treatment process [ 30 ]. Although environmental factors, such as Helicobacter pylori infection, smoking, and diet, have been proven to be risk factors, host genetics also play a key role in GC occurrence [ 31 , 32 ]. The multiformity and role of host genetics in the transcriptional active part of the genome and abnormalities in a number of cancers, including GC, have been confirmed in many studies, prompting research to identify molecular candidates for diagnosis and treatment [ 33 ].…”

Association between Toll-like receptor gene polymorphisms and risk of Helicobacter pylori infection

“…[4,5] H. pylori infection is followed by DNA damage, the repair processes and increased rate of mutations, which accelerate the development of H. pylori-related gastric cancer. [6][7][8][9][10][11] Toll-like receptors (TLRs) are cell transmembrane and pathogen-associated molecular pattern (PAMP) receptors that play an important role in the recognition of H. pylori, the activation of the first line of immunity against H. pylori. [12] So far, 10 members of TLR family have been found in human body, each member has the ability to recognize specific microbial pathogens and the initiation of innate immunity.…”