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The Gut Microbiome Modulates Colon Tumorigenesis
Recent studies have shown that individuals with colorectal cancer have an altered gut microbiome compared to healthy controls. It remains unclear whether these differences are a response to tumorigenesis or actively drive tumorigenesis. To determine the role of the gut microbiome in the development...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society of Microbiology
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892781/ https://www.ncbi.nlm.nih.gov/pubmed/24194538 http://dx.doi.org/10.1128/mBio.00692-13 |
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author | Zackular, Joseph P. Baxter, Nielson T. Iverson, Kathryn D. Sadler, William D. Petrosino, Joseph F. Chen, Grace Y. Schloss, Patrick D. |
author_facet | Zackular, Joseph P. Baxter, Nielson T. Iverson, Kathryn D. Sadler, William D. Petrosino, Joseph F. Chen, Grace Y. Schloss, Patrick D. |
author_sort | Zackular, Joseph P. |
collection | PubMed |
description | Recent studies have shown that individuals with colorectal cancer have an altered gut microbiome compared to healthy controls. It remains unclear whether these differences are a response to tumorigenesis or actively drive tumorigenesis. To determine the role of the gut microbiome in the development of colorectal cancer, we characterized the gut microbiome in a murine model of inflammation-associated colorectal cancer that mirrors what is seen in humans. We followed the development of an abnormal microbial community structure associated with inflammation and tumorigenesis in the colon. Tumor-bearing mice showed enrichment in operational taxonomic units (OTUs) affiliated with members of the Bacteroides, Odoribacter, and Akkermansia genera and decreases in OTUs affiliated with members of the Prevotellaceae and Porphyromonadaceae families. Conventionalization of germfree mice with microbiota from tumor-bearing mice significantly increased tumorigenesis in the colon compared to that for animals colonized with a healthy gut microbiome from untreated mice. Furthermore, at the end of the model, germfree mice colonized with microbiota from tumor-bearing mice harbored a higher relative abundance of populations associated with tumor formation in conventional animals. Manipulation of the gut microbiome with antibiotics resulted in a dramatic decrease in both the number and size of tumors. Our results demonstrate that changes in the gut microbiome associated with inflammation and tumorigenesis directly contribute to tumorigenesis and suggest that interventions affecting the composition of the microbiome may be a strategy to prevent the development of colon cancer. |
format | Online Article Text |
id | pubmed-3892781 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | American Society of Microbiology |
record_format | MEDLINE/PubMed |
spelling | pubmed-38927812014-01-24 The Gut Microbiome Modulates Colon Tumorigenesis Zackular, Joseph P. Baxter, Nielson T. Iverson, Kathryn D. Sadler, William D. Petrosino, Joseph F. Chen, Grace Y. Schloss, Patrick D. mBio Research Article Recent studies have shown that individuals with colorectal cancer have an altered gut microbiome compared to healthy controls. It remains unclear whether these differences are a response to tumorigenesis or actively drive tumorigenesis. To determine the role of the gut microbiome in the development of colorectal cancer, we characterized the gut microbiome in a murine model of inflammation-associated colorectal cancer that mirrors what is seen in humans. We followed the development of an abnormal microbial community structure associated with inflammation and tumorigenesis in the colon. Tumor-bearing mice showed enrichment in operational taxonomic units (OTUs) affiliated with members of the Bacteroides, Odoribacter, and Akkermansia genera and decreases in OTUs affiliated with members of the Prevotellaceae and Porphyromonadaceae families. Conventionalization of germfree mice with microbiota from tumor-bearing mice significantly increased tumorigenesis in the colon compared to that for animals colonized with a healthy gut microbiome from untreated mice. Furthermore, at the end of the model, germfree mice colonized with microbiota from tumor-bearing mice harbored a higher relative abundance of populations associated with tumor formation in conventional animals. Manipulation of the gut microbiome with antibiotics resulted in a dramatic decrease in both the number and size of tumors. Our results demonstrate that changes in the gut microbiome associated with inflammation and tumorigenesis directly contribute to tumorigenesis and suggest that interventions affecting the composition of the microbiome may be a strategy to prevent the development of colon cancer. American Society of Microbiology 2013-11-05 /pmc/articles/PMC3892781/ /pubmed/24194538 http://dx.doi.org/10.1128/mBio.00692-13 Text en Copyright © 2013 Zackular et al. http://creativecommons.org/licenses/by-nc-sa/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-ShareAlike 3.0 Unported license (http://creativecommons.org/licenses/by-nc-sa/3.0/) , which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Zackular, Joseph P. Baxter, Nielson T. Iverson, Kathryn D. Sadler, William D. Petrosino, Joseph F. Chen, Grace Y. Schloss, Patrick D. The Gut Microbiome Modulates Colon Tumorigenesis |
title | The Gut Microbiome Modulates Colon Tumorigenesis |
title_full | The Gut Microbiome Modulates Colon Tumorigenesis |
title_fullStr | The Gut Microbiome Modulates Colon Tumorigenesis |
title_full_unstemmed | The Gut Microbiome Modulates Colon Tumorigenesis |
title_short | The Gut Microbiome Modulates Colon Tumorigenesis |
title_sort | gut microbiome modulates colon tumorigenesis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892781/ https://www.ncbi.nlm.nih.gov/pubmed/24194538 http://dx.doi.org/10.1128/mBio.00692-13 |
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