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World J Gastroenterol. Jan 28, 2014; 20(4): 908-922
Published online Jan 28, 2014. doi: 10.3748/wjg.v20.i4.908
Published online Jan 28, 2014. doi: 10.3748/wjg.v20.i4.908
Inflammation and colorectal cancer, when microbiota-host mutualism breaks
Marco Candela, Silvia Turroni, Elena Biagi, Simone Rampelli, Patrizia Brigidi, Department of Pharmacy and Biotechnology, University of Bologna, 40126 Bologna, Italy
Franck Carbonero, Department of Food Science, University of Arkansas, Fayetteville, AR 72704, United States
Carla Fiorentini, Department of Therapeutic Research and Medicines Evaluation, Istituto Superiore di Sanità, 00161 Rome, Italy
Author contributions: Candela M conceived and designed the article, and wrote the manuscript; Turroni S, Biagi E, Carbonero F, Fiorentini C reviewed literature, wrote the manuscript, revised and edited the draft; Rampelli S performed bioinformatics analysis; Brigidi P reviewed and edited the final version of the article; all Authors read and approved the final version of the manuscript.
Correspondence to: Marco Candela, PhD, Department of Pharmacy and Biotechnology, University of Bologna, Via Belmeloro 6, 40126 Bologna, Italy. marco.candela@unibo.it
Telephone: +39-51-2099727 Fax: +39-51-2099734
Received: September 27, 2013
Revised: November 26, 2013
Accepted: December 12, 2013
Published online: January 28, 2014
Processing time: 121 Days and 2.2 Hours
Revised: November 26, 2013
Accepted: December 12, 2013
Published online: January 28, 2014
Processing time: 121 Days and 2.2 Hours
Core Tip
Core tip: By performing the co-abundance groups analysis of the publicly available datasets from microbiome surveys in colorectal cancer (CRC) patients, we have been successful in identifying pro-carcinogenic and protective groups of microorganisms, showing the potential to modulate the fate of CRC onset and progression. Possible mechanisms involved in microbiota-dependent carcinogenesis are reviewed, and the central role of inflammation as a trigger forcing the microbiota from a mutualistic configuration to a CRC-promoting asset is discussed. Finally, possible intervention strategies for modulating microbiome in order to preserve its mutualistic configuration along life span are suggested.