Insights into Gastric Carcinogenesis:From Helicobacter pylori infection to gastric cancer

Despite major advances in GC research, several key questions remain unresolved. Gastric carcinogenesis is a multistep process shaped by premalignant mucosal changes, chronic inflammation, bacterial virulence factors, and altered host-cell signaling. Although H. pylori infection is the main etiological driver of non-cardia GC, only a minority of infected individuals ultimately develop malignancy, indicating that additional inflammatory, bacterial, and host-related factors determine disease progression. This thesis investigates gastric carcinogenesis from four complementary perspectives. First, it addresses the detection of premalignant gastric lesions, with a focus on serological biomarkers that may support risk stratification and surveillance. Second, it examines systemic inflammatory mediators that may link chronic infection to malignant transformation. Third, it explores host-cell regulation of the H. pylori virulence factor CagA, providing insight into bacterial mechanisms that may disturb epithelial signaling. Finally, it investigates the role of protein tyrosine phosphatases, LMWPTP and PTP1B, in established GC. By integrating these themes, this thesis aims to improve understanding of GC development, early detection, and progression.