Fig. 4

Colonization of the stomach with cagA-positive H. pylori strains and progression to DLBCL. Following long-term colonization of the bacterium in stomach mucosa, CagA protein is secreted into cells via T4SS. Upon entrance of CagA, intracellular CagA-SHP2 complex is formed. Although there is probably no association between the CagA and progression of PGL to MALT lymphoma, this complex potentially stimulates the lymphogenesis process and ultimately DLBCL by activating on ERK1, ERK2, p38MAPKs, BCL2, and NF-κB, as well as inhibiting p53 or the JAK-STAT signaling pathway. It also damages DNA and microRNA by producing reactive oxygen and nitrogen species (RONS)