Evidence map›Paper›PMID 34950835›Full record

ArticleJBMR plus2021

Vitamin D and Breast Cancer: Mechanistic Update.

JoEllen Welsh

Open access · goldAbstract read
In one paragraph

Article in JBMR plus, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.2field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. PRIMA-1ACS omega · 2023
    Article
  15. Vitamin K2 enhances the tumor suppressive effects of 1,25(OH)The Journal of steroid biochemistry and molecular biology · 2023
    Article
  16. Observational
  17. Article
  18. Review
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 WelshDepartment of Environmental Health Sciences SUNY Albany Cancer Research Center Rensselaer NY USA.ORCID https://orcid.org/0000-0001-7025-7889
University at Albany, State University of New York · US

Funding

Vitamin D and HA Signaling in TNBCR01CA194500 · NCI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI WELSH, JOELLEN · 2015 to 2019
$2.2M
Vitamin D, Metabolic Flux and Breast CancerR21CA166434 · NCI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI WELSH, JOELLEN · 2013 to 2014
$354k
BIO-ACTIVATION OF VITAMIN D IN MAMMARY GLANDR03CA103018 · NCI · UNIVERSITY OF NOTRE DAME · PI WELSH, JOELLEN · 2003 to 2004
$149k
NCI NIH HHS R01 CA194500NCI NIH HHS R03 CA103018NCI NIH HHS R21 CA166434
6 · The paper itself

Abstract

The presence of the vitamin D receptor (VDR) in mammary gland and breast cancer has long been recognized, and multiple preclinical studies have demonstrated that its ligand, 1,25-dihydroxyvitamin D (1,25D), modulates normal mammary gland development and inhibits growth of breast tumors in animal models. Vitamin D deficiency is common in breast cancer patients, and some evidence suggests that low vitamin D status enhances the risk for disease development or progression. Although many 1,25D-responsive targets in normal mammary cells and in breast cancers have been identified, validation of specific targets that regulate cell cycle, apoptosis, autophagy, and differentiation, particularly in vivo, has been challenging. Model systems of carcinogenesis have provided evidence that both VDR expression and 1,25D actions change with transformation, but clinical data regarding vitamin D responsiveness of established tumors is limited and inconclusive. Because breast cancer is heterogeneous, the relevant VDR targets and potential sensitivity to vitamin D repletion or supplementation will likely differ between patient populations. Detailed analysis of VDR actions in specific molecular subtypes of the disease will be necessary to clarify the conflicting data. Genomic, proteomic, and metabolomic analyses of in vitro and in vivo model systems are also warranted to comprehensively understand the network of vitamin D-regulated pathways in the context of breast cancer heterogeneity. This review provides an update on recent studies spanning the spectrum of mechanistic (cell/molecular), preclinical (animal models), and translational work on the role of vitamin D in breast cancer. © 2021 The Author.

Indexed as

CANCERCELL/TISSUE SIGNALING—ENDOCRINE PATHWAYSNUTRITIONPTH/VIT D/FGF23

Identifiers

PMID34950835
PMCPMC8674767
OpenAlexW3211512462

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.