Streptococcus anginosus in the development and treatment of precancerous lesions of gastric cancer

Table 1 Microorganisms associated with precancerous lesions of gastric cancer

Microorganisms	Primary site	Potential mechanism	Ref.
Helicobacter pylori	Gastrointestinal tract, oral	Cytotoxin-associated gene A and vacuolar cytotoxin A cause DNA damage. increased genetic instability leads to mutations	Salvatori et al[71]
			Malfertheiner et al[72]
Streptococcus Anginosus	Oral, nasopharyngeal, gastrointestinal tract, vaginal	The streptococcal surface protein TMPC interacts with ANXA2-mediated attachment and colonization. Spontaneously induces progressive chronic gastritis, atrophy, heterotrophic hyperplasia	Fu et al[73]
			Stasiewicz and Karpiński[74]
EBV	Oropharynx, blood, lymphatic system and other tissues and organs	Viral proteins inducing methylation, regulating host gene expression and malignant transformation	Yang et al[75]
		EBV driving DNA hypermethylation, frequent PIK3CA mutations, and the overexpression of JAK2, PD-L1, and PD-L2	Iizasa et al[47]
Candida albicans	Skin, oral, gastrointestinal tract	Reduces the diversity and abundance of fungi in the stomach; destroys the mucosal epithelium, produces carcinogens, triggers chronic inflammation, induces Th17 immune responses, among other mechanisms	Yu and Liu[49]
			Zhong et al[50]
Others	Gastrointestinal tract, oral, etc.	Homogeneity and diversity of the gastric microbiota; the inflammatory response; dysbiosis of the gastric microbiota favors invasion and growth of pathogens and disrupts the mucosal barrier	Stewart et al[37]
			Liao et al[76]

EBV: Epstein-Barr virus.