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Review
. 2016 Sep 8:70:395-411.
doi: 10.1146/annurev-micro-102215-095513.

Gut Microbiota, Inflammation, and Colorectal Cancer

Caitlin A Brennan  1 , Wendy S Garrett  1   2   3   4
Affiliations
Review

Gut Microbiota, Inflammation, and Colorectal Cancer

Caitlin A Brennan et al. Annu Rev Microbiol. .

Abstract

Colorectal cancer is the second-leading cause of cancer-related deaths in the United States and fourth-leading cause of cancer-related deaths worldwide. While cancer is largely considered to be a disease of genetic and environmental factors, increasing evidence has demonstrated a role for the microbiota (the microorganisms associated with the human body) in shaping inflammatory environments and promoting tumor growth and spread. Herein, we discuss both human data from meta'omics analyses and data from mechanistic studies in cell culture and animal models that support specific bacterial agents as potentiators of tumorigenesis-including Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, and colibactin-producing Escherichia coli. Further, we consider how microbes can be used in diagnosing colorectal cancer and manipulating the tumor environment to encourage better patient outcomes in response to immunotherapy treatments.

Keywords: Fusobacterium; colitis; colorectal cancer; inflammation; microbiota/microbiome; mucosal immunology.

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Figures

Figure 1
Figure 1
Microbes with well-characterized roles in the development of specific cancers (34, 73, 74).
Figure 2
Figure 2
Progression of colorectal cancer development from normal epithelium to an invasive carcinoma.
Figure 3
Figure 3
Cross talk among environmental and genetic factors with the microbe-inflammation-cancer axis.
Figure 4
Figure 4
The future of microbiota theranostics.
See this image and copyright information in PMC

References

    1. Arpaia N, Campbell C, Fan X, Dikiy S, van der Veeken J, et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature. 2013;504(7480):451–55. - PMC - PubMed
    1. Arthur JC, Perez-Chanona E, Mühlbauer M, Tomkovich S, Uronis JM, et al. Intestinal inflammation targets cancer-inducing activity of the microbiota. Science. 2012;338(6103):120–23. Distinguished the roles of colibactin-producing E. coli in inflammation and tumorigenesis using animal models. - PMC - PubMed
    1. Atarashi K, Tanoue T, Ando M, Kamada N, Nagano Y, et al. Th17 cell induction by adhesion of microbes to intestinal epithelial cells. Cell. 2015;163(2):367–80. - PMC - PubMed
    1. Atarashi K, Tanoue T, Shima T, Imaoka A, Kuwahara T, et al. Induction of colonic regulatory T cells by indigenous Clostridium species. Science. 2011;331(6015):337–41. - PMC - PubMed
    1. Ballal SA, Veiga P, Fenn K, Michaud M, Kim JH, et al. Host lysozyme-mediated lysis of Lactococcus lactis facilitates delivery of colitis-attenuating superoxide dismutase to inflamed colons. Proc. Natl. Acad. Sci. USA. 2015;112(25):7803–8. - PMC - PubMed

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