Evidence map›Paper›PMID 28317533›Full record

ReviewDermatologic clinics2017

Genetics of Vitiligo.

Richard A Spritz, Genevieve H L Andersen

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

Review in Dermatologic clinics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 5 pooled it
7.4field-weighted citation impact, top 2% 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

95 citing papers in PubMed, 5 syntheses or guidelines pooled it, 190 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Vitiligo.Nature reviews. Disease primers · 2025
    Review
  16. Article
  17. The Role of Functional Polymorphisms of ApoptoticIranian journal of medical sciences · 2025
    Article
  18. Article
  19. Article
  20. Vitiligo.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025
    Review

35 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

2 authors at 1 institution in 1 country.

Richard A SpritzHuman Medical Genetics and Genomics Program, University of Colorado School of Medicine, 12800 East 19th Avenue, Room 3100, MS8300, Aurora, CO 80045, USA. Electronic address: richard.spritz@ucdenver.edu.
Genevieve H L AndersenHuman Medical Genetics and Genomics Program, University of Colorado School of Medicine, 12800 East 19th Avenue, Room 3100, MS8300, Aurora, CO 80045, USA.
University of Colorado Anschutz Medical Campus · US

Funding

VitGene International Consortium to Identify Susceptibility Genes for GeneralizedR01AR056292 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SPRITZ, RICHARD ANDREW · 2008 to 2016
$6.9M
VitiligoR01AR045584 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SPRITZ, RICHARD ANDREW · 1999 to 2014
$6.2M
Identification and Functional Analyses of Common and Rare Causal Variants in SLAR01AR065951 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SPRITZ, RICHARD ANDREW · 2014 to 2016
$1.2M
NIAMS NIH HHS R01 AR045584NIAMS NIH HHS R01 AR056292NIAMS NIH HHS R01 AR065951
6 · The paper itself

Abstract

Vitiligo reflects simultaneous contributions of multiple genetic risk factors and environmental triggers. Genomewide association studies have discovered approximately 50 genetic loci contributing to vitiligo risk. At many vitiligo susceptibility loci, the relevant genes and DNA sequence variants are identified. Many encode proteins involved in immune regulation, several play roles in cellular apoptosis, and others regulate functions of melanocytes. Although many of the specific biologic mechanisms need elucidation, it is clear that vitiligo is an autoimmune disease involving a complex relationship between immune system programming and function, aspects of the melanocyte autoimmune target, and dysregulation of the immune response.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisApoptosis Regulatory ProteinsAutoimmunityCTLA-4 AntigenForkhead Transcription FactorsGenetic Predisposition to DiseaseHLA-A2 AntigenHLA-DR4 AntigenHumansMelanocytesNLR ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 22Receptor, Platelet-Derived Growth Factor alphaVitiligoAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCTLA-4 AntigenCTLA4 protein, humanForkhead Transcription FactorsFOXD3 protein, humanHLA-A2 AntigenHLA-DR4 AntigenNLRP1 protein, humanNLR ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanReceptor, Platelet-Derived Growth Factor alphaAutoimmunityGeneGenetic epidemiologyGenetic linkageGenomewide association studyVitiligo

Identifiers

PMID28317533
PMCPMC5362127
OpenAlexW2596110276

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.