Gut mucosal microbiome across stages of colorectal carcinogenesis
Gut microbial dysbiosis contributes to the development of colorectal cancer (CRC). Here we catalogue the microbial communities in human gut mucosae at different stages of colorectal tumorigenesis. We analyse the gut mucosal microbiome of 47 paired samples of adenoma and adenoma-adjacent mucosae, 52...
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| Published in | Nature communications Vol. 6; no. 1; p. 8727 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
30.10.2015
Nature Publishing Group Nature Pub. Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2041-1723 2041-1723 |
| DOI | 10.1038/ncomms9727 |
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| Abstract | Gut microbial dysbiosis contributes to the development of colorectal cancer (CRC). Here we catalogue the microbial communities in human gut mucosae at different stages of colorectal tumorigenesis. We analyse the gut mucosal microbiome of 47 paired samples of adenoma and adenoma-adjacent mucosae, 52 paired samples of carcinoma and carcinoma-adjacent mucosae and 61 healthy controls. Probabilistic partitioning of relative abundance profiles reveals that a metacommunity predominated by members of the oral microbiome is primarily associated with CRC. Analysis of paired samples shows differences in community configurations between lesions and the adjacent mucosae. Correlations of bacterial taxa indicate early signs of dysbiosis in adenoma, and co-exclusive relationships are subsequently more common in cancer. We validate these alterations in CRC-associated microbiome by comparison with two previously published data sets. Our results suggest that a taxonomically defined microbial consortium is implicated in the development of CRC.
Changes in gut microbial communities contribute to the development of colorectal cancer. Here, the authors analyse the gut mucosal microbiome of patients and healthy subjects and identify distinct microbial consortia associated with different stages of colorectal cancer tumorigenesis. |
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| AbstractList | Gut microbial dysbiosis contributes to the development of colorectal cancer (CRC). Here we catalogue the microbial communities in human gut mucosae at different stages of colorectal tumorigenesis. We analyse the gut mucosal microbiome of 47 paired samples of adenoma and adenoma-adjacent mucosae, 52 paired samples of carcinoma and carcinoma-adjacent mucosae and 61 healthy controls. Probabilistic partitioning of relative abundance profiles reveals that a metacommunity predominated by members of the oral microbiome is primarily associated with CRC. Analysis of paired samples shows differences in community configurations between lesions and the adjacent mucosae. Correlations of bacterial taxa indicate early signs of dysbiosis in adenoma, and co-exclusive relationships are subsequently more common in cancer. We validate these alterations in CRC-associated microbiome by comparison with two previously published data sets. Our results suggest that a taxonomically defined microbial consortium is implicated in the development of CRC. Gut microbial dysbiosis contributes to the development of colorectal cancer (CRC). Here we catalogue the microbial communities in human gut mucosae at different stages of colorectal tumorigenesis. We analyse the gut mucosal microbiome of 47 paired samples of adenoma and adenoma-adjacent mucosae, 52 paired samples of carcinoma and carcinoma-adjacent mucosae and 61 healthy controls. Probabilistic partitioning of relative abundance profiles reveals that a metacommunity predominated by members of the oral microbiome is primarily associated with CRC. Analysis of paired samples shows differences in community configurations between lesions and the adjacent mucosae. Correlations of bacterial taxa indicate early signs of dysbiosis in adenoma, and co-exclusive relationships are subsequently more common in cancer. We validate these alterations in CRC-associated microbiome by comparison with two previously published data sets. Our results suggest that a taxonomically defined microbial consortium is implicated in the development of CRC. Changes in gut microbial communities contribute to the development of colorectal cancer. Here, the authors analyse the gut mucosal microbiome of patients and healthy subjects and identify distinct microbial consortia associated with different stages of colorectal cancer tumorigenesis. Gut microbial dysbiosis contributes to the development of colorectal cancer (CRC). Here we catalogue the microbial communities in human gut mucosae at different stages of colorectal tumorigenesis. We analyse the gut mucosal microbiome of 47 paired samples of adenoma and adenoma-adjacent mucosae, 52 paired samples of carcinoma and carcinoma-adjacent mucosae and 61 healthy controls. Probabilistic partitioning of relative abundance profiles reveals that a metacommunity predominated by members of the oral microbiome is primarily associated with CRC. Analysis of paired samples shows differences in community configurations between lesions and the adjacent mucosae. Correlations of bacterial taxa indicate early signs of dysbiosis in adenoma, and co-exclusive relationships are subsequently more common in cancer. We validate these alterations in CRC-associated microbiome by comparison with two previously published data sets. Our results suggest that a taxonomically defined microbial consortium is implicated in the development of CRC.Gut microbial dysbiosis contributes to the development of colorectal cancer (CRC). Here we catalogue the microbial communities in human gut mucosae at different stages of colorectal tumorigenesis. We analyse the gut mucosal microbiome of 47 paired samples of adenoma and adenoma-adjacent mucosae, 52 paired samples of carcinoma and carcinoma-adjacent mucosae and 61 healthy controls. Probabilistic partitioning of relative abundance profiles reveals that a metacommunity predominated by members of the oral microbiome is primarily associated with CRC. Analysis of paired samples shows differences in community configurations between lesions and the adjacent mucosae. Correlations of bacterial taxa indicate early signs of dysbiosis in adenoma, and co-exclusive relationships are subsequently more common in cancer. We validate these alterations in CRC-associated microbiome by comparison with two previously published data sets. Our results suggest that a taxonomically defined microbial consortium is implicated in the development of CRC. |
| ArticleNumber | 8727 |
| Author | Nakatsu, Geicho Ng, Siew Chien Tsoi, Ho Dong, Yujuan Sheng, Jianqiu He, Yuqi Wong, Sunny Hei Wang, Kunning Liang, Qiaoyi Zhou, Haokui Wu, William Ka Kai Zhang, Jingwan Li, Xiangchun Kang, Qian Cao, Lei Sung, Joseph J. Y. Yu, Jun Zhang, Ning |
| Author_xml | – sequence: 1 givenname: Geicho surname: Nakatsu fullname: Nakatsu, Geicho organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 2 givenname: Xiangchun surname: Li fullname: Li, Xiangchun organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 3 givenname: Haokui surname: Zhou fullname: Zhou, Haokui organization: Department of Microbiology, The Chinese University of Hong Kong – sequence: 4 givenname: Jianqiu surname: Sheng fullname: Sheng, Jianqiu organization: Department of Gastroenterology, Beijing Military General Hospital – sequence: 5 givenname: Sunny Hei orcidid: 0000-0002-3354-9310 surname: Wong fullname: Wong, Sunny Hei organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 6 givenname: William Ka Kai surname: Wu fullname: Wu, William Ka Kai organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute, Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong – sequence: 7 givenname: Siew Chien surname: Ng fullname: Ng, Siew Chien organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 8 givenname: Ho surname: Tsoi fullname: Tsoi, Ho organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 9 givenname: Yujuan surname: Dong fullname: Dong, Yujuan organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 10 givenname: Ning surname: Zhang fullname: Zhang, Ning organization: Department of Gastroenterology, The First Affiliated Hospital of Sun Yat-sen University – sequence: 11 givenname: Yuqi orcidid: 0000-0001-8930-2117 surname: He fullname: He, Yuqi organization: Department of Gastroenterology, Beijing Military General Hospital – sequence: 12 givenname: Qian surname: Kang fullname: Kang, Qian organization: Department of Gastroenterology, Beijing Military General Hospital – sequence: 13 givenname: Lei surname: Cao fullname: Cao, Lei organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 14 givenname: Kunning surname: Wang fullname: Wang, Kunning organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 15 givenname: Jingwan surname: Zhang fullname: Zhang, Jingwan organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 16 givenname: Qiaoyi surname: Liang fullname: Liang, Qiaoyi organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 17 givenname: Jun surname: Yu fullname: Yu, Jun email: junyu@cuhk.edu.hk organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute – sequence: 18 givenname: Joseph J. Y. surname: Sung fullname: Sung, Joseph J. Y. email: jjysung@cuhk.edu.hk organization: Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, CUHK Shenzhen Research Institute |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26515465$$D View this record in MEDLINE/PubMed |
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| Snippet | Gut microbial dysbiosis contributes to the development of colorectal cancer (CRC). Here we catalogue the microbial communities in human gut mucosae at... |
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| Title | Gut mucosal microbiome across stages of colorectal carcinogenesis |
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