Evidence map›Paper›PMID 20347977›Full record

ArticleThe Journal of steroid biochemistry and molecular biology2010

Tumor progression in the LPB-Tag transgenic model of prostate cancer is altered by vitamin D receptor and serum testosterone status.

Sarah Mordan-McCombs, Theodore Brown, Wei-Lin Winnie Wang, Ann-Christin Gaupel, Joellen Welsh, Martin Tenniswood

Abstract read
In one paragraph

Article in The Journal of steroid biochemistry and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
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

21 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Non-Musculoskeletal Benefits of Vitamin D beyond the Musculoskeletal System.International journal of molecular sciences · 2021
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Vitamin D Signaling Suppresses Early Prostate Carcinogenesis in TgAPTCancer prevention research (Philadelphia, Pa.) · 2019
    Article
  9. Review
  10. Review
  11. Extraskeletal actions of vitamin D.Annals of the New York Academy of Sciences · 2016
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Cellular and molecular effects of vitamin D on carcinogenesis.Archives of biochemistry and biophysics · 2012
    Review
  17. Review
  18. Article
  19. Article
  20. Vitamin d, sunlight and prostate cancer risk.Advances in preventive medicine · 2011
    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

6 authors at 2 institutions in 1 country.

Sarah Mordan-McCombsCancer Research Center, Department of Biomedical Sciences, School of Public Health, State University of New York at Albany, Rensselaer, NY 12144, United States.
Theodore Brown
Wei-Lin Winnie Wang
Ann-Christin Gaupel
Joellen Welsh
Martin Tenniswood
University at Albany, State University of New York · USUniversity of Notre Dame · US

Funding

PROSTATE CANCER, CALCIUM AND VITAMIN DR01CA101114 · NCI · UNIVERSITY OF NOTRE DAME · PI WELSH, JOELLEN · 2003 to 2007
$1.6M
NCI NIH HHS R01 CA101114NCI NIH HHS R01 CA101114-01
6 · The paper itself

Abstract

Previous studies have suggested that 1,25 dihydroxyvitamin D(3) (1,25(OH)2D3) induces cell cycle arrest and/or apoptosis in prostate cancer cells in vitro, suggesting that vitamin D may be a useful adjuvant therapy for prostate cancer and a chemopreventive agent. Most epidemiological data however shows a weak link between serum 25(OH)D3 and risk of prostate cancer. To explore this dichotomy we have compared tumor progression in the LPB-Tag model of prostate in VDR knock out (VDRKO) and wild type (VDRWT) mice. On the C57BL/6 background LPB-Tag tumors progress significantly more rapidly in the VDRKO mice. VDRKO tumors show significantly higher levels of cell proliferation than VDRWT tumors. In mice supplemented with testosterone to restore the serum levels to the normal range, these differences in tumor progression, and proliferation are abrogated, suggesting that there is considerable cross-talk between the androgen receptor (AR) and the vitamin D axis which is reflected in significant changes in steady state mRNA levels of the AR, PCNA, cdk2 survivin and IGFR1 and 2 genes. These alterations may explain the differences between the in vitro data and the epidemiological studies.

Indexed as

AnimalsAnticarcinogenic AgentsAntineoplastic AgentsApoptosisCalcifediolCyclin-Dependent Kinase 2Disease ProgressionHumansInhibitor of Apoptosis ProteinsMaleMiceMice, TransgenicProliferating Cell Nuclear AntigenProstatic NeoplasmsReceptor, IGF Type 1Receptors, AndrogenAnticarcinogenic AgentsAntineoplastic AgentsBirc5 protein, mouseCalcifediolCdk2 protein, mouseCyclin-Dependent Kinase 2Inhibitor of Apoptosis ProteinsProliferating Cell Nuclear AntigenReceptor, IGF Type 1Receptors, AndrogenReceptors, CalcitriolRepressor ProteinsSurvivinTestosterone

Identifiers

PMID20347977
PMCPMC4211603
OpenAlexW2076659431

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.