| Cancer | Bacteria inducing cancer | Mechanisms of carcinogenesis | References |
| Gallbladder cancer | Salmonella typhi | Changes in the sequence of p53 gene; activation of protein kinase; cytolethal distending toxin B (CdtB); biliary deoxycholate; cholic acid derivatives; 5-alpha,6-alpha-epoxide cholesterol; upregulation of the PI3K pathway | [8, 10–13] | Lung cancer | Chlamydia pneumoniae | Alteration in apoptosis and/or cell programming signalling; overexpression of miRNA-328; by stimulating lung-resident γδ T cells; development of Myd88-dependent IL-1b and IL-23; generation of reactive oxygen species; increased secretion of cytokines, IL-8, IL-10, and TNF | [5, 19–24] | Colorectal cancer | Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis, Enterococcus faecalis, Clostridium septicum, Fusobacterium spp., and Escherichia coli | Secretion of Bacteroides fragilis toxin; activation of NF-μB; expression of IL-17A, and TNF-α; β-catenin expression, induction of IL-17R, NF-κB, and Stat3 signals; induction of the gene expression of colibactin (clbB) and Bacteroides fragilis toxin (BFT), increased colonial interleukin-17, and colonic epithelial DNA damage | [69, 72–75] | Breast cancer | Methylobacterium radiotolerans, Sphingomonas yanoikuyae | Microbiota secretes bioactive metabolites including estrogens, short-chain fatty acids, amino acid metabolites, or secondary bile acids; dysbiosis | [78, 79] | Bladder cancer | Staphylococcus albus hemolytic, Staphylococcus aureus, Klebsiella spp., Proteus mirabilis, and E. coli | Formation of N-nitrosamines; DNA methylation; reactive chemical species | [83–87] |
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