Intestinal Inflammation Targets Cancer-Inducing Activity of the Microbiota

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Science  05 Oct 2012:
Vol. 338, Issue 6103, pp. 120-123
DOI: 10.1126/science.1224820

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Of Microbes and Cancer

Inflammation is a well-established driver of tumorigenesis. For example, patients with inflammatory bowel disease have an elevated risk of developing colorectal cancer (CRC). Whether the gut microbiota also contributes to the development of CRC is less well understood. Arthur et al. (p. 120, published online 16 August; see the Perspective by Schwabe and Wang) now show that the microbiota does indeed promote tumorigenesis in an inflammation-driven model of CRC in mice. Although germ-free mice were protected against developing cancer, colonization of mice with Escherichia coli was sufficient to drive tumorigenesis.


Inflammation alters host physiology to promote cancer, as seen in colitis-associated colorectal cancer (CRC). Here, we identify the intestinal microbiota as a target of inflammation that affects the progression of CRC. High-throughput sequencing revealed that inflammation modifies gut microbial composition in colitis-susceptible interleukin-10–deficient (Il10−/−) mice. Monocolonization with the commensal Escherichia coli NC101 promoted invasive carcinoma in azoxymethane (AOM)–treated Il10−/− mice. Deletion of the polyketide synthase (pks) genotoxic island from E. coli NC101 decreased tumor multiplicity and invasion in AOM/Il10−/− mice, without altering intestinal inflammation. Mucosa-associated pks+ E. coli were found in a significantly high percentage of inflammatory bowel disease and CRC patients. This suggests that in mice, colitis can promote tumorigenesis by altering microbial composition and inducing the expansion of microorganisms with genotoxic capabilities.

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