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Microbiome, inflammation and colorectal cancer.

Abstract
Chronic inflammation is linked to the development of multiple cancers, including those of the colon. Inflammation in the gut induces carcinogenic mutagenesis and promotes colorectal cancer initiation. Additionally, myeloid and lymphoid cells infiltrate established tumors and propagate so called "tumor-elicited inflammation", which in turn favors cancer development by supporting the survival and proliferation of cancer cells. In addition to the interaction between cancer cells and tumor infiltrating immune cells, the gut also hosts trillions of bacteria and other microbes, whose roles in colorectal inflammation and cancer have only been appreciated in the past decade or so. Commensal and pathobiotic bacteria promote colorectal cancer development by exploiting tumor surface barrier defects following cancer initiation, by invading normal colonic tissue and inducing local inflammation, and by generating genotoxicity against colonic epithelial cells to accelerate their oncogenic transformation. On the other hand, a balanced population of microbiota is important for the prevention of colorectal cancer due to their roles in providing certain bacterial metabolites and inhibiting intestinal inflammation. In this review we summarize our current knowledge regarding the link between microbiota, inflammation, and colorectal cancer, and aim to delineate the mechanisms by which gut microbiome and inflammatory cytokines regulate colorectal tumorigenesis.
AuthorsJu Chen, Elise Pitmon, Kepeng Wang
JournalSeminars in immunology (Semin Immunol) Vol. 32 Pg. 43-53 (08 2017) ISSN: 1096-3618 [Electronic] England
PMID28982615 (Publication Type: Journal Article, Review)
CopyrightPublished by Elsevier Ltd.
Chemical References
  • Cytokines
  • Inflammation Mediators
Topics
  • Animals
  • Carcinogenesis
  • Colorectal Neoplasms (immunology)
  • Cytokines (metabolism)
  • Gastrointestinal Microbiome (immunology)
  • Humans
  • Inflammation (immunology)
  • Inflammation Mediators (metabolism)
  • Microbiota (immunology)
  • Symbiosis

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