Table 1. Helicobacter pylori virulence factors and further consequences to GC development.

	Risk Factors Action	Consequences	Authors
H. pylori virulence factors	Activation and secretion of cytokines in epithelial cells such as IL-8 by cag pathogenicity island (cagPAI)	• CagPAI- and inflammation-driven cancerogenesis • Codetermination of the risk for gastric cancer	Stein et al., 2017 [86]
	Influence of CagA on the tumor suppressor function of apoptosis-stimulating protein of p53 (ASPP2)	• The interaction between CagA and ASPP2 • The consequent degradation of p53 • Increased risk of gastric cancer	Buti et al., 2011 [87]
	CagA-dependent loss of polarity and activation of aberrant Erk signalling after the delivery into epithelial cells	• Senescence and mitogenesis in epithelial cells, both nonpolarized and polarized	Saito et al., 2010 [92]
	East Asian-type CagA has a higher binding affinity for the Src homology-2 domain-containing phosphatase 2 (SHP2)	• Greater risk of peptic ulcer development and/or gastric cancer when compared to its Western counterpart	Hatakeyama et al., 2004; Higashi et al., 2002; Jones et al., 2009; Vilaichone et al., 2004 [95–98]
	CagA-positive strains with EPIYA motifs; Strains possessing cagA with an EPIYA-D segment (an East Asian-type cagA-positive strain)	• Reduction variety of intracellular signalling systems after the infection of gastric epithelial cells; • Higher risk of gastric cancer among infected individuals	Yamaoka et al., 2010; Backert et al., 2001 [100, 101]