Helicobacter pylori, gastric microbiota and gastric cancer relationship: Unrolling the tangle

Figure 1 Possible mechanisms involved (A) in the etiology of non-cardiac gastric cancer (intestinal type) resulting in the classical cascade of Correa histopathological precancerous lesions (B) as seen in an upper gastrointestinal endoscopy. Hp-I: Helicobacter pylori infection; GC: Gastric cancer; PPIs: Proton pump inhibitors; CagA: Cytotoxin-associated gene A; VacA: Vacuolating cytotoxin A; GGT: γ-glutamyl transpeptidase; BabA: Blood-group-antigen-binding adhesin; SabA: Sialic acid-binding adhesin; OipA: Outer inflammatory protein; NapA: Neutrophil activation protein A; EMT: Epithelial-mesenchymal transition; ROS/RNS: Reactive oxygen species/Reactive nitrogen species; EGFR: Epidermal growth factor receptor; SPEM: Spasmolytic polypeptide-expressing metaplasia; CSC: Cancer stem cell; BMDSCs: Bone marrow-derived stem cells; IEN: Intraepithelial neoplasia.