Helicobacter pylori infection induced genome instability and gastric cancer

Abstract

Genome stability and integrity are constantly challenged by exogenous insults such as bacterial infections. When genome stability is perturbed, oncogenic transformation can ensue. Helicobacter pylori (H. pylori) infection is a driving factor of gastric cancer, which is the third leading cause of cancer-related mortality worldwide. Mechanistically, H. pylori infection drives inflammation and directly or indirectly induces DNA damage such as oxidative damage and double-strand breaks (DSBs) in host cells. In addition, the resulting genetic and/or epigenetic perturbations alter the choice of DNA repair pathways. These changes result in imprecise DNA repair, genomic instability as well as chromosomal aberrations that eventually lead to gastric carcinogenesis. In this review, we summarize the mechanisms how H. pylori infection cause DNA damage and alter the DNA damage response pathways in host cells. We highlight the relationship between H. pylori infection and genomic instability that can lead to gastric cancer and propose a potential strategy to interrupt gastric carcinogenesis.

Distinct genomic profile in h. pylori‐associated gastric cancer

“…TMB was similar among non-MSI subtypes, but H. pyloripositive gastric tumors had a lower MSI score. Consistent with a previous report, H. pylori infection is associated with double-strand break and reduced DNA repair efficiency in gastric cancer, 22 which is evident from the mutational signatures seen in H. pylori-positive tumor. Furthermore, we also found APOBEC-associated mutational signature in this subtype, which could be caused by H. pylori-induced mutagenesis.…”

Risk assessment of gastric cancer in the presence of Helicobacter pylori cagA and hopQII genes

“…pylori is basically a type of spiral bacteria, but it can also be spherical, habitable and pathogenic, but cannot be cultured (in vitro) and attached to the gastric mucosa (generally there are two forms. Biological and Pathogenic Sick) (3,4).…”

IS200/IS605 Family-Associated TnpB Increases Transposon Activity and Retention

“…Transposable elements (TEs) are mobile DNA sequences that can move around or create copies of themselves in an organism's genome (1). TEs are major contributors to disease, development, and evolution (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). As significant sources of mutations, revealing their network of interactions and dynamics is a key factor in understanding the dynamics of evolution.…”