Table 1.

Different pathogenic bacteria/bacterial clades, their possible mode of action, and cancer types with these bacteria. List is not exhaustive, but brings out some common modes of action by different bacterial clades in pathogenesis of different cancers.

Bacteria/Clade	Mode of Action	Cancer
Helicobacter pylori	Disruption of stomach and colonic epithelial integrity creates a niche in stomach suitable for further pathogenic bacterial invasion [40].	Stomach and colorectal.
Fusobacterium nucleatum	Suspension of disintegration of β-catenin signalling, increased expression of TLR4 activation of p21- activated kinase and cyclin D1 [41], increased inflammatory gene expression, and suppression of antitumour NKT cells via effector molecules FadA and Fap2 [42,43].	Stomach, colorectal, oral, and lung.
Bacteroides fragilis	Reactive-oxygen-species (ROS) generation leading to DNA damage, colon-epithelial-barrier disruption, and depletion of mucous membrane, causing increased inflammation [44,45,46].	Stomach, colorectal, and lung.
Pathogenic Escherichia coli	Toxin colibactin indirectly induces release of growth factors in tumour microenvironment; cytotoxic necrotizing factor (CNF)-mediated disruption of host cell DNA repair mechanism [47,48].	Stomach and lung.
Salmonella sp.	Stabilises and prevents degradation of β-catenin by deubiquitinase activity of its AvrA protein [49,50,51].	Stomach, colorectal, gall-bladder, and lung.
Peptostreptococcus anaerobius	Increases expression of SREB2 gene via ROS, causing increased cholesterol biosynthesis in colon [52].	Colorectal.
Citrobacter rodentium	Loss of cell polarity, depletion of epithelial barrier, and increased inflammation [53].	Colorectal.
Mycobacterium tuberculosis, Streptococcus viridans, Haemophilus influenza, Streptococcus pnuemoniae, Staphyloccocus	Involved in various chronic inflammatory lung disorders like asthma, cystic fibrosis, and chronic obstructive pulmonary disease; potential for accelerating tumourigenesis via inflammatory cytokines like tumour necrosis factor [54,55,56].	Lung.
Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans	Reach pancreas from oral cavity through blood circulation and act as secondary drivers of cancer; impair host innate immunity, leading to increased colonisation by other bacteria, leading to chronic inflammation of pancreas causing accelerated tumourigenesis [57,58,59].	Pancreatic.
Proteobacteria, Betaproteobacteria, Firmicutes, Alcaligenaceae, Burkholderiales	Alter metabolism and oestrogen recycling, and exert pressure on immune system [38].	Breast.
P. gingivalis and Tannerella forsythia	Cause overexpression of inflammatory cytokines; gingipain K produced by P. gingivalis paralyses immune cells, and induce indirect overexpression of glucose-transporter (GLUT-1 and GLUT-4) genes that help in faster tumour-cell proliferation [60,61,62,63].	Oesophageal.