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. 2017 Dec 28;23(48):8626-8650.
doi: 10.3748/wjg.v23.i48.8626.

Fusobacterium's link to colorectal neoplasia sequenced: A systematic review and future insights

Affiliations

Fusobacterium's link to colorectal neoplasia sequenced: A systematic review and future insights

Hisham Hussan et al. World J Gastroenterol. .

Abstract

Aim: To critically evaluate previous scientific evidence on Fusobacterium's role in colorectal neoplasia development VSports手机版. .

Methods: Two independent investigators systematically reviewed all original scientific articles published between January, 2000, and July, 2017, using PubMed, EMBASE, and MEDLINE V体育安卓版. A total of 355 articles were screened at the abstract level. Of these, only original scientific human, animal, and in vitro studies investigating Fusobacterium and its relationship with colorectal cancer (CRC) were included in the analysis. Abstracts, review articles, studies investigating other colonic diseases, and studies written in other languages than English were excluded from our analysis. Ninety articles were included after removing duplicates, resolving disagreements between the two reviewers, and applying the above criteria. .

Results: Studies have consistently identified positive associations between Fusobacterium, especially Fusobacterium nucleatum (F. nucleatum), and CRC. Stronger associations were seen in CRCs proximal to the splenic flexure and CpG island methylator phenotype (CIMP)-high CRCs. There was evidence of temporality and a biological gradient, with increased F. nucleatum DNA detection and quantity along the traditional adenoma-carcinoma sequence and in CIMP-high CRC precursors. Diet may have a differential impact on colonic F. nucleatum enrichment; evidence suggests that high fiber diet may reduce the risk of a subset of CRCs that are F. nucleatum DNA-positive. Data also suggest shorter CRC and disease-specific survival with increased amount of F. nucleatum DNA in CRC tissue. The pathophysiology of enrichment of F. nucleatum and other Fusobacterium species in colonic tissue is unclear; however, the virulence factors and changes to the local colonic environment with disruption of the protective mucus layer may contribute. The presence of a host lectin (Gal-GalNAc) in the colonic epithelium may also mediate F. nucleatum attachment to CRC and precursors through interaction with an F. nucleatum protein, fibroblast activation protein 2 (FAP2). The clinical significance of detection or enrichment of Fusobacterium in colorectal neoplasia is ambiguous, but data suggest a procarcinogenic effect of F. nucleatum, likely due to activation of oncogenic and inflammatory pathways and modulation of the tumor immune environment. This is hypothesized to be mediated by certain F. nucleatum strains carrying invasive properties and virulence factors such as FadA and FAP V体育ios版. .

Conclusion: Evidence suggests a potential active role of Fusobacterium, specifically F VSports最新版本. nucleatum, in CRC. Future prospective and experimental human studies would fill an important gap in this literature. .

Keywords: Carcinogenesis; Colon microbiota; Colorectal cancer; Colorectal polyps; Fusobacterium; Fusobacterium nucleatum; Systematic; review. V体育平台登录.

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Conflict of interest statement (VSports app下载)

Conflict-of-interest statement: The authors do not have any relevant conflicts of interest (including relevant financial interests, activities, relationships, and/or affiliations).

Figures

Figure 1
Figure 1
Diagram illustrating systematic review flow and methods.
Figure 2
Figure 2
A simplified figure illustrating the link between Fusobacterium nucleatum and colorectal cancer. A: Association between Fusobacterium nucleatum (F. nucleatum) and colorectal cancer (CRC) pathways and location; B: F. nucleatum prevalence along chromosomal instability (CIN) and the CpG island methylator phenotype (CIMP)-high CRC pathways and their precursors; C: Postulated mechanisms of F. nucleatum induced colorectal carcinogenesis.

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