Early screening and risk factors for gastric cancer

Figure 1 Mechanism of H. pylori-induced gastric cancer. A: The Correa cascade illustrates the histopathological progression from normal gastric mucosa to gastric cancer over time; B: Molecular mechanisms of H. pylori infection, highlighting key virulence factors and signaling pathways (e.g., signal transducer and activator of transcription 3, nuclear factor-κB, mitogen-activated protein kinase/extracellular signal-regulated kinase, phosphoinositide 3-kinases/protein kinase B, β-catenin) that promote cytoskeleton rearrangement, loss of cell polarity, and enhanced migration/invasion, ultimately contributing to gastric cancer development. STAT3: Signal transducer and activator of transcription 3; NF-κB: Nuclear factor-κB; MAPK: Mitogen-activated protein kinase; ERK: Extracellular signal-regulated kinase; Akt: Protein kinase B; PI3K: Phosphoinositide 3-kinases; H. pylori: H. pylori.