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Original article
The oral microbiota in colorectal cancer is distinctive and predictive


Background and aims Microbiota alterations are linked with colorectal cancer (CRC) and notably higher abundance of putative oral bacteria on colonic tumours. However, it is not known if colonic mucosa-associated taxa are indeed orally derived, if such cases are a distinct subset of patients or if the oral microbiome is generally suitable for screening for CRC.

Methods We profiled the microbiota in oral swabs, colonic mucosae and stool from individuals with CRC (99 subjects), colorectal polyps (32) or controls (103).

Results Several oral taxa were differentially abundant in CRC compared with controls, for example, Streptococcus and Prevotellas pp. A classification model of oral swab microbiota distinguished individuals with CRC or polyps from controls (sensitivity: 53% (CRC)/67% (polyps); specificity: 96%). Combining the data from faecal microbiota and oral swab microbiota increased the sensitivity of this model to 76% (CRC)/88% (polyps). We detected similar bacterial networks in colonic microbiota and oral microbiota datasets comprising putative oral biofilm forming bacteria. While these taxa were more abundant in CRC, core networks between pathogenic, CRC-associated oral bacteria such as Peptostreptococcus, Parvimonas and Fusobacterium were also detected in healthy controls. High abundance of Lachnospiraceae was negatively associated with the colonisation of colonic tissue with oral-like bacterial networks suggesting a protective role for certain microbiota types against CRC, possibly by conferring colonisation resistance to CRC-associated oral taxa and possibly mediated through habitual diet.

Conclusion The heterogeneity of CRC may relate to microbiota types that either predispose or provide resistance to the disease, and profiling the oral microbiome may offer an alternative screen for detecting CRC.

  • colonic bacteria
  • colorectal cancer
  • colorectal cancer screening
  • diet
  • tumour markers

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  • Contributors BF: study concept and design, acquisition of data, analysis and interpretation of data, drafting of the manuscript, critical revision of the manuscript for important intellectual content, statistical analysis and study supervision. RDW and MPB: acquisition of data. KC, AD and IBJ: CRC classifier development. EH: study concept and design. MO: study concept and design and acquisition of data. FS and PWO: study concept and design, drafting of the manuscript, critical revision of the manuscript for important intellectual content, obtained funding and study supervision.

  • Funding The authors are funded in part by Science Foundation Ireland (APC/SFI/12/RC/2273) in the form of a research centre, the APC Microbiome Institute. IBJ is supported by a Science Foundation Ireland grant (13/SIRG/2128).

  • Disclaimer The authors are funded in part by Science Foundation Ireland (APC/SFI/12/RC/2273) in the form of a research centre which is/has recently been in receipt of research grants from the following companies: Cremo, Mead Johnson Nutrition,Kerry, General Mills, GE Healthcare, Friesland Campina, Sigmoid, Alimentary Health, Second Genome, Nutricia, Danone, Janssen, AbbVie, Suntory Morinaga Milk Industry Ltd, Pfizer Consumer Health, Radisens, 4D Pharma, Crucell, Adare Pharma, Artugen Therapeutics, Caelus. FS isa founder shareholder in Atlantia Food Clinical Trials, Tucana Health and Alimentary Health Ltd. PWOT and IBJ are founder shareholders of Tucana Health. These relationships with industry have no bearing on the present work and neither influenced nor constrained it.

  • Ethics approval University Ethics Committee.

  • Provenance and peer review Not commissioned; internally peer reviewed.

  • Data sharing statement All sequencing data will be available upon request.

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