4.7 Review

The inflammatory pathogenesis of colorectal cancer

Journal

NATURE REVIEWS IMMUNOLOGY
Volume 21, Issue 10, Pages 653-667

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41577-021-00534-x

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Funding

  1. Georg-Speyer-Haus
  2. LOEWE Center Frankfurt Cancer Institute (FCI) - Hessen State Ministry for Higher Education, Research and the Arts [III L 5-519/03/03.001-(0015)]
  3. Deutsche Forschungsgemeinschaft [FOR2438: Gr1916/11-1, SFB 815, SFB 1177, SFB 1292, GRK 2336]
  4. German Federal Ministry of Health
  5. Ministry of Higher Education, Research and the Arts of the State of Hessen (HMWK)

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The research on colorectal cancer indicates the importance of an inflammatory microenvironment for tumorigenesis, which influences the activation of immune cells and stromal cells, as well as the role of intestinal microbiome in tumor development. Chronic inflammation can initiate tumorigenesis, and tumor-elicited and therapy-induced inflammation are also implicated in promoting colorectal cancer.
The mutational landscape of colorectal cancer (CRC) does not enable predictions to be made about the survival of patients or their response to therapy. Instead, studying the polarization and activation profiles of immune cells and stromal cells in the tumour microenvironment has been shown to be more informative, thus making CRC a prototypical example of the importance of an inflammatory microenvironment for tumorigenesis. Here, we review our current understanding of how colon cancer cells interact with their microenvironment, comprised of immune cells, stromal cells and the intestinal microbiome, to suppress or escape immune responses and how inflammatory processes shape the immune pathogenesis of CRC. Mark Schmitt and Florian Greten describe the mechanisms by which chronic inflammation can initiate tumorigenesis and by which tumour-elicited and therapy-induced inflammation can promote colorectal cancer, as well as the role of extrinsic factors such as diet, the microbiota and the mycobiota.

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