Evidence map›Paper›PMID 36408538›Full record

ReviewExperimental biology and medicine (Maywood, N.J.)2023

Bile acids as carcinogens in the colon and at other sites in the gastrointestinal system.

Harris Bernstein, Carol Bernstein

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Experimental biology and medicine (Maywood, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Ultra-processed Foods and Gastrointestinal Cancer: Epidemiologic Evidence, Mechanistic Pathways, and Clinical Implications.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Review
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  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
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  16. Review
  17. Article
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  19. Review
  20. Pangenome Analysis ofMicroorganisms · 2025
    Article
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

2 authors at 1 institution in 1 country.

Harris BernsteinDepartment of Cellular and Molecular Medicine, College of Medicine, University of Arizona, Tucson, AZ 85724-5044, USA.
Carol BernsteinDepartment of Cellular and Molecular Medicine, College of Medicine, University of Arizona, Tucson, AZ 85724-5044, USA.ORCID 0000-0001-7761-6565
University of Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer incidence is associated with a high-fat diet. Such a diet is linked to elevated levels of bile acids in the gastrointestinal system and the circulation. Secondary bile acids are produced by microorganisms present at high concentrations in the colon. Recent prospective studies and a retrospective study in humans associate high circulating blood levels of secondary bile acids with increased risk of colon cancer. Feeding mice a diet containing a secondary bile acid, so their feces have the bile acid at a level comparable to that in the feces of humans on a high-fat diet, also causes colon cancer in the mice. Studies using human cells grown in culture illuminate some mechanisms by which bile acids cause cancer. In human cells, bile acids cause oxidative stress leading to oxidative DNA damage. Increased DNA damage increases the occurrence of mutations and epimutations, some of which provide a cellular growth advantage such as apoptosis resistance. Cells with such mutations/epimutations increase by natural selection. Apoptosis, or programmed cell death, is a beneficial process that eliminates cells with unrepaired DNA damage, whereas apoptosis-resistant cells are able to survive DNA damage using inaccurate repair processes. This results in apoptosis-resistant cells having more frequent mutations/epimutations, some of which are carcinogenic. The experiments on cultured human cells have provided a basis for understanding at the molecular level the human studies that recently reported an association of bile acids with colon cancer, and the mouse studies showing directly that bile acids cause colon cancer. Similar, but more limited, findings of an association of dietary bile acids with other cancers of the gastrointestinal system suggest that understanding the role of bile acids in colon carcinogenesis may contribute to understanding carcinogenesis in other organs.

Indexed as

Bile Acids and SaltsColonic NeoplasmsAnimalsCarcinogenesisCarcinogensHumansMiceRetrospective StudiesBile Acids and SaltsCarcinogensapoptosisCarcinogenesisDNA damagegastrointestinal canceroxidative stress

Identifiers

PMID36408538
PMCPMC9989147
OpenAlexW4309506721

What Socratic 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 Socratic graph.