Gastric organoids: A promising model for studying “inflammation-cancer” transition in atrophic gastritis

Figure 4 Molecular and cellular mechanisms driving “inflammation-cancer” transition in atrophic gastritis. H. pylori: Helicobacter pylori; P13K: Phosphoinositide 3-kinase; AKT: Protein kinase B; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; IL: Interleukin; MAPK: Mitogen-activated protein kinase; ERK: Extracellular signal-regulated kinase; JNK: C-Jun N-terminal kinase; SHP-2: Src homology-2 domain-containing phosphatase 2; ROS: Reactive oxygen species; Nrf2: Nuclear factor erythroid-2-related factor 2; HIF: Hypoxia inducible factor; PD-L1: Programmed death-ligand 1; CTLA-4: Cytotoxic T lymphocyte-associated protein 4; TAMs: Tumor-associated macrophages; CAF: Cancer-associated fibroblasts; ECM: Extracellular matrix; EMT: Epithelial-mesenchymal transition; TME: Tumor microenvironment.