Table 2.

Representative bacteria in different types of tumors.

Cancer Types	Microbes	Levels	Pro-Tumor Mechanisms	Ref.
Breast	Fusobacterium nucleatum	Increased	Suppresses T cell infiltration into tumors; promotes tumor growth and metastatic progression	[29]
	Anaerococcus, Caulobacter Propionibacterium, Streptococcus, Staphylococcus	Decreased	Positively correlated with oncogenic immune features and T-cell activation-related genes	[9]
Bile duct	Bifidobacteriaceae, Enterobacteriaceae, Enterococcaceae	Increased	Increased production of bile acids and ammonia, leading to DNA damage in host cells and carcinogenesis	[88]
Cervical	Fusobacterium spp.	Increased	Associated with increased IL-4 and TGF-β1 mRNA in cervical cells	[89]
	Anaerotruncus, Anaerostipes, Atopobium, Arthrospira, Bacteroides, Dialister, Peptoniphilus, Porphyromonas, Ruminococcus, Treponema	Increased	Elevates vaginal pH to weaken host defense against infection and promotes tumor formation	[90]
Colorectal	Bacteroides fragilis	Increased	Increased interleukin-17 in the colon and DNA damage in the colonic epithelium, accelerating tumor onset and elevating host mortality	[91]
	Fusobacterium	Increased	Cancer cell proliferation and distant metastasis	[80]
Esophageal	Lactobacillus fermentum	Increased	Establishes acidic environment for growth advantage	[92]
	Helicobacter pylori	Increased	Spread from gastric colonization	[92]
	Campylobacter spp.	Increased	Causes inflammation that could contribute to carcinogenesis	[93]
	Porphyromonas gingivalis	Increased	Accelerates cell cycle and promotes cellular migration and metabolism of potentially carcinogenic substances such as ethanol to the carcinogenic derivative acetaldehyde	[94]
Extrahepatic Bile duct	Helicobacter pylori	Increased	Increases abundance of the virulence genes cagA and vacA and promotes tumor formation	[89]
	Helicobacter bilis	Increased	Induces inflammation to contribute to tumor formation	[95]
Gallbladder	Fusobacterium nucleatum, Escherichia coli, Enterobacter spp.	Increased	Promotes gallstone development and chronic cholecystitis to contribute to tumor formation	[96]
Gastric	Helicobacter pylori	Increased	CagA protein suppresses p53-mediated apoptosis of host cells while increasing cell motility and metastatic phenotypes	[97]
	Fusobacterium nucleatum	Increased	Induces epithelial-to-mesenchymal transition	[98]
Liver cancer	Helicobacter bifidus	Increased	Contributes to formation of chronic hepatitis that promotes tumor progression	[99]
Lung	Acidovorax spp.	Increased	Associated with carcinomas with p53 mutations	[100]
	Thermus, Legionella	Increased	Associated with advanced-stage and metastatic cancer	[101]
Oral cancer	Fusobacterium nucleatum	Increased	Induces epithelial-to-mesenchymal transition	[98]
	Firmicutes (esp. Streptococcus), Actinobacteria (esp. Rothia)	Increased	Elevated in normal oral tissues	[102]
Ovarian	Mycoplasma	Increased	Prevalent in 60% of tumors	[103]
Pancreatic	Enterobacteriaceae, Pseudomonas spp., Mycobacterium avium, Pseudoxanthomonas, Streptomyces, Bacillus cereus	Increased	Contributes to chemotherapy resistance and immune suppression	[104,105]
	Malassezia globosa	Increased	Induces the complement cascade through the activation of mannose-binding lectin C3 to promote tumorigenesis	[106]
Prostate	Pseudomonas, Escherichia, Immunobacterium, Propionibacterium spp.	Increased	Induces prostatitis and differentiation of prostate basal cells into ductal cells to promote tumor formation	[107]
	Propionibacterium acnes spp.	Increased	Induces prostatitis and promotes tumor formation	[108]
	Staphylococcus	Increased	Induces inflammation of the prostate tissue and promotes tumor formation	[107]
	Fusobacterium nucleatum, Streptococcus oligosporus	Increased	Induces chemoresistance by regulating autophagy	[109]