Emerging roles of the microbiome in cancer
Open accessAbstract
Gene-environment interactions underlie cancer susceptibility and progression. Yet, we still have limited knowledge of which environmental factors are important and how they function during tumorigenesis. In this respect, the microbial communities that inhabit our gastrointestinal tract and other body sites have been unappreciated until recently. However, our microbiota are environmental factors that we are exposed to continuously, and human microbiome studies have revealed significant differences in the relative abundance of certain microbes in cancer cases compared with controls. To characterize the function of microbiota in carcinogenesis, mouse models of cancer have been treated with antibiotics. They have also been maintained in a germfree state or have been colonized with specific bacteria in specialized (gnotobiotic) facilities. These studies demonstrate that microbiota can increase or decrease cancer susceptibility and progression by diverse mechanisms such as by modulating inflammation, influencing the genomic stability of host cells and producing metabolites that function as histone deacetylase inhibitors to epigenetically regulate host gene expression. One might consider microbiota as tractable environmental factors because they are highly quantifiable and relatively stable within an individual compared with our exposures to external agents. At the same time, however, diet can modulate the composition of microbial communities within our gut, and this supports the idea that probiotics and prebiotics can be effective chemoprevention strategies. The trajectory of where the current work is headed suggests that microbiota will continue to provide insight into the basic mechanisms of carcinogenesis and that microbiota will also become targets for therapeutic intervention.
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Abnormal diversity (dysbiosis) in the gut has been proven to be associated with human diseases such as obesity, inflammatory bowel disease, and cancer.
“Abnormal diversity (dysbiosis) in the gut has been proven to be associated with human diseases, such as obesity, inflammatory bowel disease, cancer, etc. 20,21,33,34”
From The Diversity of Gut Microbiome is Associated With Favorable Responses to Anti–Programmed Death 1 Immunotherapy in Chinese Patients With NSCLC (2019) · cites this paper as [20]
The metagenomic-studies section (page unavailable) describes dysbiosis and reports microbiome differences in Crohn’s disease; its discussion of colorectal tumors also supports an association with cancer. The obesity evidence in the cited passages concerns mice, so it does not establish the claimed association between gut dysbiosis and obesity in humans. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe gut microbiota may produce or transform molecules affecting host metabolism, gut barrier integrity, xenobiotics and drug metabolism, protection against gastro-intestinal pathogens, and host immune system modulation.
“In fact, it has been widely studied that the gut microbiota may produce or transform molecules affecting several aspects of human health, including: host’s metabolism modulation, gut barrier integrity maintenance, xenobiotics and drug metabolism, protection against gastro-intestinal pathogens and host’s immune system modulation [31,32,33,34].”
From Gut Microbiota and Cancer: From Pathogenesis to Therapy (2019) · cites this paper as [33]
Preclinical studies using germ-free mice models demonstrated that the gut microbiome can deeply affect cancer genesis and progression through different mechanisms.
“In line with that, many preclinical studies performed using germ-free mice models demonstrated how the gut microbiome is able to deeply affect cancer genesis and progression through different mechanisms [33,54,55].”
From Gut Microbiota and Cancer: From Pathogenesis to Therapy (2019) · cites this paper as [33]
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- Authors
- Bultman, S. J.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Bultman, S. J.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-12-03
- Volume
- 35
- Issue
- 2
- Pages
- 249-255
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- PMC
- PMC3908754
- OpenAlex
- W2097944779
- Cited by
- 239
- References
- 115
- Citations by year
- 2026: 11 · 2025: 9 · 2024: 21 · 2023: 15 · 2022: 18 · 2021: 21 · 2020: 20 · 2019: 21 · 2018: 24 · 2017: 24 · 2016: 22 · 2015: 19 · 2014: 13
- FWCI
- 1.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Carcinogenesis (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- National Institutes of Health
- National Cancer Institute (CA125237, R01CA125237)
- National Institute of Environmental Health Sciences (P30ES010126)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
- Keywords
- gut microbiota, cancer susceptibility, gene-environment interaction, inflammation, genome stability, histone deacetylase inhibitors, epigenetic regulation, diet, probiotics, prebiotics, chemoprevention, germ-free mice, gnotobiotic mice, antibiotic therapy
- MeSH terms
- Animals, Anti-Bacterial Agents, Humans, Neoplasms, Gastrointestinal Tract, Mice, Microbiota
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