Epidemiology of Helicobacter pylori and CagA-Positive Infections and Global Variations in Gastric Cancer

Gastric cancer is a major health burden and is the fifth most common malignancy and the third most common cause of death from cancer worldwide. Development of gastric cancer involves several aspects, including host genetics, environmental factors, and infection. There is increasing evidence from epidemiological studies of the association of infection and specific virulence factors with gastric cancer. Studies in animal models indicate is a primary factor in the development of gastric cancer. One major virulence factor in is the cytotoxin-associated gene A ( ), which encodes the CagA protein in the pathogenicity island ( PAI). Meta-analysis of studies investigating CagA seropositivity irrespective of status identified that CagA seropositivity increases the risk of gastric cancer (OR = 2.87, 95% CI: 1.95⁻4.22) relative to the risk of infection alone (OR = 2.31, 95% CI: 1.58⁻3.39). Eradicating is a strategy for reducing gastric cancer incidence. A meta-analysis of six randomised controlled trials (RCTs) suggests that searching for and eradicating infection reduces the subsequent incidence of gastric cancer with a pooled relative risk of 0.66 (95% CI: 0.46⁻0.95). The introduction in regions of high gastric cancer incidence of population-based screening and treatment programmes, with a scientifically valid assessment of programme processes, feasibility, effectiveness and possible adverse consequences, would impact the incidence of -induced gastric cancer. Given the recent molecular understanding of the oncogenic role of CagA, targeting screening and treatment programmes in populations with a high prevalence of CagA-positive strains, particularly the more oncogenic East Asian CagA strains, may be worth further investigation to optimise the benefits of such strategies.