Evidence map›Paper›PMID 19610133›Full record

ArticleWorld journal of gastroenterology2009

Bile acids as endogenous etiologic agents in gastrointestinal cancer.

Harris Bernstein, Carol Bernstein, Claire M Payne, Katerina Dvorak

Open access · bronzeAbstract readEditorial
In one paragraph

Article in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed, 4 pooled it
6.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

184 citing papers in PubMed, 4 syntheses or guidelines pooled it, 327 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Review
  9. Bile Acid Metabolism as a Unifying Readout for Diet, Microbiome Function, and Gastrointestinal Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  10. Article
  11. Review
  12. Gut microbiota in health and disease.Molecular biomedicine · 2026
    Review
  13. Prediagnostic Plasma Metabolite Profiles and Prediction of Hepatocellular Carcinoma Risk: The Multiethnic Cohort.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Extracellular vesicles as indicators of environmental stress response inExtracellular vesicles and circulating nucleic acids · 2026
    Article
  20. Article

124 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Harris Bernstein
Carol Bernstein
Claire M Payne
Katerina Dvorak
University of Pittsburgh · USSouthern Arizona VA Health Care System · USUniversity of Arizona · US

Funding

SPORE in Gastrointestinal CancerP50CA095060 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2002 to 2012
$25.3M
Preventive of Bile Acid-Induced Colonic Oxidative DNA DamageR01CA119087 · NCI · UNIVERSITY OF ARIZONA · PI PAYNE, CLAIRE MARGARET · 2006 to 2010
$1.3M
Cytochrome C Oxidase I:A Biomarker for Colon Cancer RiskR21CA111513 · NCI · UNIVERSITY OF ARIZONA · PI PAYNE, CLAIRE MARGARET · 2005 to 2006
$256k
NCI NIH HHS 1 P50CA95060NCI NIH HHS 5 R01 CA119087NCI NIH HHS P50 CA095060NCI NIH HHS R01 CA119087NCI NIH HHS R21 CA111513NCI NIH HHS R21CA111513-01A1
6 · The paper itself

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.

Indexed as

Cell Transformation, NeoplasticAnimalsApoptosisBile Acids and SaltsCarcinogensDNA DamageFemaleGastrointestinal NeoplasmsHumansMaleReactive Oxygen SpeciesReceptors, Cytoplasmic and NuclearRisk FactorsBile Acids and SaltsCarcinogensReactive Oxygen SpeciesReceptors, Cytoplasmic and Nuclear

Identifiers

PMID19610133
PMCPMC2712893
OpenAlexW2160363801

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.