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Bile acids as endogenous etiologic agents in gastrointestinal cancer
Open accessAbstract
Bile acids are implicated as etiologic agents in cancer of the gastrointestinal (GI) tract, including cancer of the esophagus, stomach, small intestine, liver, biliary tract, pancreas and colon/rectum. Deleterious effects of bile acid exposure, likely related to carcinogenesis, include: induction of reactive oxygen and reactive nitrogen species; induction of DNA damage; stimulation of mutation; induction of apoptosis in the short term, and selection for apoptosis resistance in the long term. These deleterious effects have, so far, been reported most consistently in relation to esophageal and colorectal cancer, but also to some extent in relation to cancer of other organs. In addition, evidence is reviewed for an association of increased bile acid exposure with cancer risk in human populations, in specific human genetic conditions, and in animal experiments. A model for the role of bile acids in GI carcinogenesis is presented from a Darwinian perspective that offers an explanation for how the observed effects of bile acids on cells contribute to cancer development.
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“Secondary bile acids might contribute to development of CRC because they generate reactive oxygen and nitrogen species that cause DNA damage and promote resistance to apoptosis.160”
From Influence of the Gut Microbiome, Diet, and Environment on Risk of Colorectal Cancer (2020) · cites this paper as [160]
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Metadata
- Authors
- Bernstein, H., Bernstein, C., Payne, C. M., & Dvorak, K.
- Affiliations
- Atrium Health Wake Forest Baptist (US)
- Corresponding author
- Dvorak, Katerina
- Venue
- World Journal of Gastroenterology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2009
- Volume
- 15
- Issue
- 27
- Pages
- 3329
- ISSN
- 1007-9327 (ISSN-L)
- PMC
- PMC2712893
- OpenAlex
- W2160363801
- Cited by
- 340
- References
- 174
- Citations by year
- 2026: 18 · 2025: 30 · 2024: 23 · 2023: 27 · 2022: 29 · 2021: 25 · 2020: 13 · 2019: 16 · 2018: 32 · 2017: 13 · 2016: 16 · 2015: 16 · 2014: 20 · 2013: 19 · 2012: 13
- FWCI
- 14.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- World Journal of Gastroenterology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Arizona Biomedical Research Commission
- National Institutes of Health (5r21ca111513-02)
- National Cancer Institute (R01CA119087, R21 CA111513, 1P50 CA 95060, R21CA111513-01A1, P50CA095060)
- Topics
- Health Sciences › Medicine › Surgery › Cholangiocarcinoma and Gallbladder Cancer Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Health Sciences › Medicine › Surgery › Esophageal Cancer Research and Treatment
- Keywords
- bile acids, gastrointestinal cancer, carcinogenesis, esophageal cancer, colorectal cancer, reactive oxygen species, reactive nitrogen species, DNA damage, apoptosis, apoptosis resistance, cancer risk
- MeSH terms
- Animals, Bile Acids and Salts, Carcinogens, Cell Transformation, Neoplastic, DNA Damage, Female, Gastrointestinal Neoplasms, Humans, Male, Risk Factors, Apoptosis, Reactive Oxygen Species, Receptors, Cytoplasmic and Nuclear
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