Helicobacter Pylori and Gastric Carcinogenesis: Mechanisms, Clinical Implications, and Preventive Strategies

Helicobacter pylori is a spiral shaped Gram-negative bacterium that colonizes the human stomach and persists for decades when untreated. Infection is common worldwide, especially in East Asia and parts of South America, and it is the strongest established risk factor for non-cardia gastric adenocarcinoma. In 1994 the International Agency for Research on Cancer classified the organism as a Group I carcinogen, which placed a common bacterial infection at the center of cancer prevention. The pathway from infection to carcinoma proceeds along Correas cascade, beginning with chronic active gastritis and advancing through atrophic gastritis, intestinal metaplasia, dysplasia, and invasive cancer. Carcinogenesis reflects an interplay between virulence factors such as CagA and VacA, persistent inflammation with immune evasion, and durable epigenetic and genomic injury that remodels transcriptional programs in the gastric epithelium. Clinical evidence indicates that eradication therapy reduces cancer incidence, although benefit declines once advanced precancerous changes are established. This review synthesizes mechanistic and clinical data, outlines the epidemiology and pathology of infection associated with cancer, assesses the impact of eradication at individual and population levels, and evaluates diagnostics and risk markers that can focus surveillance. It also considers challenges that include antibiotic resistance and microbiome consequences, and it discusses future directions such as precision prevention, biomarker-based triage, and vaccine development. A coherent strategy that integrates molecular understanding with public health practice can reduce the global burden of gastric cancer in diverse settings.