期刊
SCIENCE
卷 359, 期 6375, 页码 592-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aah3648
关键词
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资金
- Bloomberg Philanthropies
- NIH [R01 CA151393, K08 DK087856, 5T32CA126607-05, P30 DK089502, P30 CA006973, P50 CA62924]
- Alexander and Margaret Stewart Trust (Johns Hopkins University School of Medicine)
- American Society of Colon and Rectal Surgeons [GSRRIG-015]
- Netherlands Organization for Scientific Research [NWO 825.11.03, 016.166.089]
- Institute Merieux
- Bristol-Myers Squibb
- Compugen
- Ervaxx
- Potenza
- Bristol-Myers Squibb Co-International Immuno-Oncology Network-IION Resource Model [300-2344]
Individuals with sporadic colorectal cancer (CRC) frequently harbor abnormalities in the composition of the gut microbiome; however, the microbiota associated with precancerous lesions in hereditary CRC remains largely unknown. We studied colonic mucosa of patients with familial adenomatous polyposis (FAP), who develop benign precursor lesions (polyps) early in life. We identified patchy bacterial biofilms composed predominately of Escherichia coli and Bacteroides fragilis. Genes for colibactin (clbB) and Bacteroides fragilis toxin (bft), encoding secreted oncotoxins, were highly enriched in FAP patients' colonic mucosa compared to healthy individuals. Tumor-prone mice cocolonized with E. coli (expressing colibactin), and enterotoxigenic B. fragilis showed increased interleukin-17 in the colon and DNA damage in colonic epithelium with faster tumor onset and greater mortality, compared to mice with either bacterial strain alone. These data suggest an unexpected link between early neoplasia of the colon and tumorigenic bacteria.
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