Abstract
The oxygen-derived free radicals that are released from activated neutrophils are one of the cytotoxic factors of Helicobacter pylori-induced gastric mucosal injury. Increased cytidine deaminase activity in H. pylori-infected gastric tissues promotes the accumulation of various mutations and might promote gastric carcinogenesis. Cytotoxin-associated gene A (CagA) is delivered into gastric epithelial cells via bacterial type IV secretion system, and it causes inflammation and activation of oncogenic pathways. H. pylori infection induces epigenetic transformations, such as aberrant promoter methylation in tumor-suppressor genes. Aberrant expression of microRNAs is also reportedly linked to gastric tumorogenesis. Moreover, recent advances in molecular targeting therapies provided a new interesting weapon to treat advanced gastric cancer through anti-human epidermal growth factor receptor 2 (HER-2) therapies. This updated review article highlights possible mechanisms of gastric carcinogenesis including H. pylori-associated factors.
Highlights
Helicobacter pylori infection is one of the most prevalent infectious diseases worldwide and 40–50% of the global human population is estimated to be infected
Cytotoxin-associated gene A (CagA), that is translocated into CD44v9-positive gastric cancer stem-like cells, which are characterized by reactive oxygen species (ROS) resistance that results from their rich GSH content, is thought to escape ROS-dependent autophagy, resulting in gastric carcinogenesis [16]
Phase III GRANITE-1 study evaluated the efficacy of mammalian target of rapamycin (mTOR) inhibitor everolimus compared to the best supportive care in patients with advanced gastric cancer that progressed after initial chemotherapy
Summary
Helicobacter pylori infection is one of the most prevalent infectious diseases worldwide and 40–50% of the global human population is estimated to be infected. Eradication of H. pylori infection has been reported as an effective strategy for both the treatment of peptic ulcers and gastric mucosa-associated lymphoid tissue (MALT) lymphoma as well as prevention of gastric cancer [1,2,3]. H. pylori eradication therapy achieved a strong recommendation, because it is useful for the treatment of gastric or duodenal ulcers, treatment and prevention of H. pylori-associated diseases such as gastric cancer, and inhibition of the spread of H. pylori infection. Bacterial virulence factors, such as, cytotoxin-associated gene A (CagA), cause inflammation and activate oncogenic pathways. This paper summarizes the molecular mechanism of H. pylori-associated gastric carcinogenesis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
