Helicobacter pylori eradication and gastric cancer prevention: current evidence and future perspectives

Introduction Helicobacter pylori infection is recognized as the principal etiological factor in gastric carcinogenesis, and despite the widespread implementation of H. pylori eradication strategies, the global burden of gastric cancer remains substantial.Areas covered This review summarizes the role of H. pylori (through key bacterial survival mechanisms, epithelial colonization, immune evasion, and virulence factors that promote persistent inflammation and mucosal injury) in gastric carcinogenesis, focusing on the sequential gastric mucosal alterations described in the Correa cascade that are accompanied by activation of oncogenic signaling pathways. Relevant literature was identified from databases (including PubMed and Scopus).Expert opinion Recent translational studies have highlighted the complexity of H. pylori-related determinants of GC progression, including bacterial virulence factors, alterations in the gastric environment, gastric microbiota, and host genetic susceptibility. However, the precise mechanisms underlying each determinant are still being elucidated. Therefore, in recent clinical practice, the early detection and eradication strategies remain the most realistic and impactful interventions. In the future, eradication-focused management may shift to a more stratified model that includes earlier screening in high-risk populations, wider use of susceptibility-guided or region-adapted therapy, and molecular risk surveillance after eradication, refining recent practice.