Emerging insights in gastric cancer pathogenesis.

PURPOSE OF THE REVIEW: Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide. Although Helicobacter pylori (Hp) is a well known, leading risk factor for GC, not all patients with Hp develop malignancy, highlighting the multifactorial mechanisms involved in gastric carcinogenesis. This review summarizes recent insights into GC pathogenesis and the implications for risk stratification, screening surveillance, and prevention.

RECENT FINDINGS: Emerging evidence suggests complex interactions between microbial, genetic, environmental, and immune factors in GC pathogenesis. Chronic Hp induces irreversible changes in the gastric mucosa, underscoring the benefits of early detection and treatment. New data suggest treating Hp in younger adults may be most effective for reducing GC risk. Several microbial pathogens have been associated with GC, an evolving area of research. Recent studies also expand our understanding of hereditary and early-onset GC, including the roles of CDH1 , CTNNA1 , and homologous recombination genes. New data also highlights the contribution of environmental factors such as alcohol and acid-blocking medications on GC risk.

SUMMARY: Gastric carcinogenesis involves dynamic interactions between the gastric microbiome, host genetics, immune interactions, and environmental exposures beyond Hp infection. Improved understanding of these processes may inform prevention and early detection strategies in clinical practice.