Table 1.
Organism | Natural reservoir |
Evidence of association with CRCa | Mechanisms identified in modelsb |
Effectorsb | ||
---|---|---|---|---|---|---|
Epidemiology | Microbial enrichment |
Immune responses | ||||
Streptococcus gallolyticus | GI tract | + | − | + | Unknown | Unknown |
Enterococcus faecalis | GI tract | − | − | − | ROS-mediated DNA damage | Unknown |
Colibactin-producing Escherichia coli | GI tract | + | + | − | Toxin-mediated DNA damage | Colibactin (Pks) |
Enterotoxigenic Bacteroides fragilis | GI tract | + | + | − | Inflammation and immune-cell infiltration | Bft toxin |
Fusobacterium nucleatum | Oral cavity | + | + | − | Inflammation and immune-cell infiltration; disruption of antitumor immunity | FadA, Fap2 |
Abbreviations: CRC, colorectal cancer; GI, gastrointestinal; ROS, reactive oxygen species.
Evidence of association with CRC is based on microbial enrichment as described in the main text and epidemiological and human immune responses as described and classified in Reference 74.