Evidence map›Paper›PMID 22982628›Full record

ArticleThe Journal of steroid biochemistry and molecular biology2013

Prevention of preneoplastic lesions by dietary vitamin D in a mouse model of colorectal carcinogenesis.

Doris Maria Hummel, Ursula Thiem, Julia Höbaus, Ildiko Mesteri, Lukas Gober, Caroline Stremnitzer, João Graça, Barbara Obermayer-Pietsch, Enikö Kallay

Open access · hybridAbstract read
In one paragraph

Article in The Journal of steroid biochemistry and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Association of Vitamin D Intake,Medical sciences (Basel, Switzerland) · 2026
    Article
  4. Vitamin D is glucoprotective in aging males but not females.The Journal of steroid biochemistry and molecular biology · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. 1,25-Dihydroxyvitamin DJournal of cellular physiology · 2021
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

9 authors at 3 institutions in 2 countries.

Doris Maria HummelDepartment of Pathophysiology and Allergy Research, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria. doris.hummel@meduniwien.ac.at
Ursula Thiem
Julia Höbaus
Ildiko Mesteri
Lukas Gober
Caroline Stremnitzer
João Graça
Barbara Obermayer-Pietsch
Enikö Kallay
Medical University of Vienna · ATAstraZeneca (United Kingdom) · GBMedical University of Graz · AT

Funding

Austrian Science Fund FWF P 22200
6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the leading causes of cancer morbidity and mortality in Western countries. One of the risk factors for colorectal tumorigenesis is vitamin D insufficiency. The aim of this study was to establish whether increasing dietary vitamin D intake can prevent or delay development of chemically induced preneoplastic lesions in the colon of mice. We fed six weeks old female C57BL/6J mice (n=28) with increasing vitamin D3 concentrations (100, 400, 1000, 2500, 5000IU/kg diet). To induce dysplasia, a preneoplastic lesion, we injected mice with the carcinogen azoxymethane (10mg/kg) intraperitoneally, followed by three cycles of 2% dextran sodium sulfate salt, a tumor promoter, in the drinking water. To test our hypothesis that high vitamin D intake prevents formation of preneoplastic lesions, we have investigated the effect of increasing dietary vitamin D on development of premalignant colorectal lesions, serum 25-hydroxyvitamin D3 (25-D3) levels, and expression of renal vitamin D system genes. Dietary vitamin D concentration correlated inversely with dysplasia score (Spearman's correlation coefficient, ρ: -0.579, p=0.002) and positively with serum 25-D3 levels (ρ: 0.752, p=0.001). Increasing dietary vitamin D concentration beyond 1000IU/kg led to no further increase in circulating 25-D3 levels, while the dysplasia score leveled out at ≥2500IU/kg vitamin D. High dietary vitamin D intake led to increased renal mRNA expression of the vitamin D catabolizing enzyme cyp24a1 (ρ: 0.518, p=0.005) and decreased expression of the vitamin D activating enzyme cyp27b1 (ρ: -0.452, p=0.016), protecting the body from toxic serum levels of the active vitamin D metabolite 1,25-dihydroxyvitamin D3 (1,25-D3). Our data showed that increasing dietary vitamin D intake is able to prevent chemically induced preneoplastic lesions. The maximum impact was achieved when the mice consumed more than 2500IU vitamin D/kg diet. This article is part of a Special Issue entitled 'Vitamin D Workshop'.

Indexed as

AnimalsCholecalciferolColorectal NeoplasmsDietary SupplementsFemaleMiceMice, Inbred C57BLPrecancerous ConditionsCholecalciferol

Identifiers

PMID22982628
PMCPMC3695567
OpenAlexW1982251648

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.