Evidence map›Paper›PMID 22085499›Full record

ReviewArchives of biochemistry and biophysics2012

Cellular and molecular effects of vitamin D on carcinogenesis.

JoEllen Welsh

Open access · greenAbstract readReview
In one paragraph

Review in Archives of biochemistry and biophysics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 4 pooled it
10.5field-weighted citation impact, top 1% 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

69 citing papers in PubMed, 4 syntheses or guidelines pooled it, 161 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Serum 25-hydroxyvitamin D and breast cancer risk: a meta-analysis of prospective studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  5. Article
  6. Observational
  7. Article
  8. Biomolecules · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Vitamin DMolecules (Basel, Switzerland) · 2024
    Article
  13. Review
  14. Article
  15. PRIMA-1ACS omega · 2023
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Vitamin D as a Potential Preventive Agent For Young Women's Breast Cancer.Cancer prevention research (Philadelphia, Pa.) · 2021
    Review

9 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

1 author at 1 institution in 1 country.

JoEllen WelshCancer Research Center, University at Albany, Rensselaer, NY 12144, USA. jwelsh@albany.edu
University at Albany, State University of New York · US

Funding

VITAMIN D MEDICATED APOPTOSIS IN MAMMARY CELLSR01CA069700 · NCI · UNIVERSITY OF NOTRE DAME · PI WELSH, JOELLEN · 1995 to 2009
$2.8M
PROSTATE CANCER, CALCIUM AND VITAMIN DR01CA101114 · NCI · UNIVERSITY OF NOTRE DAME · PI WELSH, JOELLEN · 2003 to 2007
$1.6M
Bioassay for Breast Cancer PreventionRC1CA144963 · NCI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI WELSH, JOELLEN · 2009 to 2010
$996k
BIO-ACTIVATION OF VITAMIN D IN MAMMARY GLANDR03CA103018 · NCI · UNIVERSITY OF NOTRE DAME · PI WELSH, JOELLEN · 2003 to 2004
$149k
NCI NIH HHS R01 CA069700NCI NIH HHS R01 CA101114NCI NIH HHS R03 CA103018NCI NIH HHS RC1 CA144963
6 · The paper itself

Abstract

Epidemiologic data suggest that the incidence and severity of many types of cancer inversely correlates with indices of vitamin D status. The vitamin D receptor (VDR) is highly expressed in epithelial cells at risk for carcinogenesis including those resident in skin, breast, prostate and colon, providing a direct molecular link by which vitamin D status impacts on carcinogenesis. Consistent with this concept, activation of VDR by its ligand 1,25-dihydroxyvitamin D (1,25D) triggers comprehensive genomic changes in epithelial cells that contribute to maintenance of the differentiated phenotype, resistance to cellular stresses and protection of the genome. Many epithelial cells also express the vitamin D metabolizing enzyme CYP27B1 which enables autocrine generation of 1,25D from the circulating vitamin D metabolite 25-hydroxyvitamin D (25D), critically linking overall vitamin D status with cellular anti-tumor actions. Furthermore, pre-clinical studies in animal models has demonstrated that dietary supplementation with vitamin D or chronic treatment with VDR agonists decreases tumor development in skin, colon, prostate and breast. Conversely, deletion of the VDR gene in mice alters the balance between proliferation and apoptosis, increases oxidative DNA damage, and enhances susceptibility to carcinogenesis in these tissues. Because VDR expression is retained in many human tumors, vitamin D status may be an important modulator of cancer progression in persons living with cancer. Collectively, these observations have reinforced the need to further define the molecular actions of the VDR and the human requirement for vitamin D in relation to cancer development and progression.

Indexed as

AnimalsDisease Models, AnimalHumansNeoplasmsReceptors, CalcitriolVitamin DReceptors, CalcitriolVitamin D

Identifiers

PMID22085499
PMCPMC3295909
OpenAlexW2073656241

What OpenQuestion holds

Textmetadata
LicenceTDM
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.