Cited by 340Cholangiocarcinoma and Gallbladder Cancer StudiesCarcinogens and Genotoxicity AssessmentEsophageal Cancer Research and Treatment

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Bile acids as endogenous etiologic agents in gastrointestinal cancer

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Bernstein, Harris, Bernstein, Carol, Payne, Claire M, Dvorak, Katerina·2009·World Journal of Gastroenterology

DOI 10.3748/wjg.15.3329PMC PMC2712893

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Abstract

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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Authors: Bernstein, H., Bernstein, C., Payne, C. M., & Dvorak, K.
Affiliations: Atrium Health Wake Forest Baptist (US)
Corresponding author: Dvorak, Katerina
ORCID: Bernstein, Harris
Bernstein, Carol
Payne, Claire M
Venue: World Journal of Gastroenterology
Publisher: Baishideng Publishing Group Inc.
Published: 2009
Volume: 15
Issue: 27
Pages: 3329
ISSN: 1007-9327 (ISSN-L)
DOI: 10.3748/wjg.15.3329
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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Bile acids as endogenous etiologic agents in gastrointestinal cancer

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