Evidence map›Paper›PMID 25227143›Full record

ArticleEuropean journal of human genetics : EJHG2015

Identification of possible pathogenic pathways in Behçet's disease using genome-wide association study data from two different populations.

Burcu Bakir-Gungor, Elaine F Remmers, Akira Meguro, Nobuhisa Mizuki, Daniel L Kastner, Ahmet Gul, Osman U Sezerman

Open access · bronzeAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Role of Proteasomes in Inflammation.Journal of clinical medicine · 2021
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Reply to Stoimenis et al.European journal of human genetics : EJHG · 2015
    Article
  11. 'Epistatic interactions between autoimmunity and genetic thrombophilia'.European journal of human genetics : EJHG · 2015
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 3 countries.

Burcu Bakir-Gungor1] Department of Genetics and Bioinformatics, Faculty of Arts and Sciences, Bahcesehir University, Istanbul, Turkey [2] Department of Computer Engineering, Faculty of Engineering and Natural Sciences, Abdullah Gul University, Kayseri, Turkey.
Elaine F RemmersInflammatory Disease Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Akira MeguroDepartment of Ophthalmology, Yokohama City University School of Medicine, Yokohama, Kanagawa, Japan.
Nobuhisa MizukiDepartment of Ophthalmology, Yokohama City University School of Medicine, Yokohama, Kanagawa, Japan.
Daniel L KastnerInflammatory Disease Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.
Ahmet GulDivision of Rheumatology, Department of Internal Medicine, Istanbul University, Istanbul, Turkey.
Osman U SezermanBiological Sciences and Bioengineering, Faculty of Engineering and Natural Sciences, Sabanci University, Istanbul, Turkey.
National Human Genome Research Institute · USYokohama City University · JPBahçeşehir University · TRIstanbul University · TRSabancı Üniversitesi · TR

Funding

Genetics, Natural History, and Pathophysiology of Behcet's DiseaseZIAHG200374 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI KASTNER, DANIEL · 2011 to 2020
$10.5M
6 · The paper itself

Abstract

Behçet's disease (BD) is a multi-system inflammatory disorder of unknown etiology. Two recent genome-wide association studies (GWASs) of BD confirmed a strong association with the MHC class I region and identified two non-HLA common genetic variations. In complex diseases, multiple factors may target different sets of genes in the same pathway and thus may cause the same disease phenotype. We therefore hypothesized that identification of disease-associated pathways is critical to elucidate mechanisms underlying BD, and those pathways may be conserved within and across populations. To identify the disease-associated pathways, we developed a novel methodology that combines nominally significant evidence of genetic association with current knowledge of biochemical pathways, protein-protein interaction networks, and functional information of selected SNPs. Using this methodology, we searched for the disease-related pathways in two BD GWASs in Turkish and Japanese case-control groups. We found that 6 of the top 10 identified pathways in both populations were overlapping, even though there were few significantly conserved SNPs/genes within and between populations. The probability of random occurrence of such an event was 2.24E-39. These shared pathways were focal adhesion, MAPK signaling, TGF-β signaling, ECM-receptor interaction, complement and coagulation cascades, and proteasome pathways. Even though each individual has a unique combination of factors involved in their disease development, the targeted pathways are expected to be mostly the same. Hence, the identification of shared pathways between the Turkish and the Japanese patients using GWAS data may help further elucidate the inflammatory mechanisms in BD pathogenesis.

Indexed as

Genome-Wide Association StudySignal TransductionBehcet SyndromeComputational BiologyDatabases, GeneticDatasets as TopicGenetic Predisposition to DiseaseHumansJapanPhenotypePolymorphism, Single NucleotideTurkey

Identifiers

PMID25227143
PMCPMC4402634
OpenAlexW2001356797

What OpenQuestion holds

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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.