The Role of H. pylori in Gastric Carcinogenesis

Helicobacter pylori infection represents a major driver of gastric carcinogenesis, utilizing multiple mechanisms to promote tumor development. Although highly prevalent globally, only a subset of infected individuals progresses to malignancy, underscoring the importance of host–pathogen interactions in shaping disease outcomes. This chapter systematically outlines the genomic features and key virulence factors of H. pylori, such as CagA and VacA, and their roles in dysregulating critical signaling pathways, including JAK-STAT, NF-κB, and Wnt/β-catenin. We further examine how the bacterium induces oxidative stress, DNA damage, chronic inflammation, and apoptotic dysfunction, collectively fostering a tumor-permissive niche. Emerging insights into epigenetic modulation, autophagy, and microbiota dysbiosis are also highlighted. Future studies should prioritize elucidating molecular cross talk, strain heterogeneity, and novel therapeutic targets to improve clinical strategies.