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Mechanisms of Disease: inflammation and the origins of cancer

Nature Clinical Practice Oncology volume 2, pages 90–97 (2005)Cite this article

Abstract

Many common cancers develop as a consequence of years of chronic inflammation. Increasing evidence indicates that the inflammation may result from persistent mucosal or epithelial cell colonization by microorganisms; including hepatitis B virus and hepatitis C virus, which can cause hepatocellular cancer; human papilloma virus subtypes, which cause cervical cancer, and the bacterium Helicobacter pylori, which can cause gastric cancer. At present, the cause of other chronic inflammatory conditions associated with increased cancer risk, such as ulcerative colitis, is obscure. Particular microbial characteristics as well as the type of the inflammatory response contribute to clinical outcomes via influence on epithelial cell and immune responses. Persistent inflammation leads to increased cellular turnover, especially in the epithelium, and provides selection pressure that result in the emergence of cells that are at high risk for malignant transformation. Cytokines, chemokines, free radicals, and growth factors modulate microbial populations that colonize the host. Thus, therapeutic opportunities exist to target the causative microbe, the consequent inflammatory mediator, or epithelial cell responses. Such measures could be of value to reduce cancer risk in inflammation-associated malignancies.

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Figure 1: Inflammatory-epithelial interactions in multi-step carcinogenesis.
Figure 2: Gastric biopsy from a patient with chronic gastritis due to H. pylori persistence.

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Acknowledgements

Funding support, SFM: National Institutes of Health 1P20RR17695-01. MJB: National Institutes of Health RO1 GM 63270, and the Filomena D'Agostino Foundation.

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Authors and Affiliations

  1. Rhode Island Hospital,

    Steven F Moss

  2. Medicine at Brown University, Providence, Rhode Island, USA

    Steven F Moss

  3. Department of Medicine,

    Martin J Blaser

  4. New York University School of Medicine, New York, USA

    Martin J Blaser

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  1. Steven F Moss
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Correspondence to Steven F Moss.

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Glossary

CYTOKINES

Intercellular soluble proteins that activate and regulate inflammatory and immune responses through interactions with specific receptors

CHEMOKINES

Cytokines that function to recruit other inflammatory cells by chemo-attraction

FREE RADICALS

Highly reactive oxygen by-products that contain unpaired electrons, created by normal cell metabolism

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Moss, S., Blaser, M. Mechanisms of Disease: inflammation and the origins of cancer. Nat Rev Clin Oncol 2, 90–97 (2005). https://doi.org/10.1038/ncponc0081

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