Evidence map›Paper›PMID 21980439›Full record

ArticlePloS one2011

A systems genetics approach provides a bridge from discovered genetic variants to biological pathways in rheumatoid arthritis.

Hirofumi Nakaoka, Tailin Cui, Atsushi Tajima, Akira Oka, Shigeki Mitsunaga, Koichi Kashiwase, Yasuhiko Homma, Shinji Sato, Yasuo Suzuki, Hidetoshi Inoko and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. 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
1.8field-weighted citation impact, top 15% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Applications of systems approaches in the study of rheumatic diseases.The Korean journal of internal medicine · 2015
    Review
  5. Article
  6. Article
  7. Article
  8. Systems genetics in "-omics" era: current and future development.Theory in biosciences = Theorie in den Biowissenschaften · 2013
    Review
  9. Genetics and epigenetics of rheumatoid arthritis.Nature reviews. Rheumatology · 2013
    Review
  10. Article
  11. 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

11 authors at 4 institutions in 1 country.

Hirofumi NakaokaDivision of Human Genetics, Department of Integrated Genetics, National Institute of Genetics, Mishima, Shizuoka, Japan.
Tailin Cui
Atsushi Tajima
Akira Oka
Shigeki Mitsunaga
Koichi Kashiwase
Yasuhiko Homma
Shinji Sato
Yasuo Suzuki
Hidetoshi Inoko
Ituro Inoue
Tokai University · JPNational Institute of Genetics · JPJapanese Red Cross Society, Japan · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have yielded novel genetic loci underlying common diseases. We propose a systems genetics approach to utilize these discoveries for better understanding of the genetic architecture of rheumatoid arthritis (RA). Current evidence of genetic associations with RA was sought through PubMed and the NHGRI GWAS catalog. The associations of 15 single nucleotide polymorphisms and HLA-DRB1 alleles were confirmed in 1,287 cases and 1,500 controls of Japanese subjects. Among these, HLA-DRB1 alleles and eight SNPs showed significant associations and all but one of the variants had the same direction of effect as identified in the previous studies, indicating that the genetic risk factors underlying RA are shared across populations. By receiver operating characteristic curve analysis, the area under the curve (AUC) for the genetic risk score based on the selected variants was 68.4%. For seropositive RA patients only, the AUC improved to 70.9%, indicating good but suboptimal predictive ability. A simulation study shows that more than 200 additional loci with similar effect size as recent GWAS findings or 20 rare variants with intermediate effects are needed to achieve AUC = 80.0%. We performed the random walk with restart (RWR) algorithm to prioritize genes for future mapping studies. The performance of the algorithm was confirmed by leave-one-out cross-validation. The RWR algorithm pointed to ZAP70 in the first rank, in which mutation causes RA-like autoimmune arthritis in mice. By applying the hierarchical clustering method to a subnetwork comprising RA-associated genes and top-ranked genes by the RWR, we found three functional modules relevant to RA etiology: "leukocyte activation and differentiation", "pattern-recognition receptor signaling pathway", and "chemokines and their receptors".These results suggest that the systems genetics approach is useful to find directions of future mapping strategies to illuminate biological pathways.

Indexed as

Genetic TechniquesAnimalsArthritis, RheumatoidGene Regulatory NetworksGenetic LociGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansMiceModels, GeneticProtein Interaction MapsSystems Biology

Identifiers

PMID21980439
PMCPMC3182219
OpenAlexW2051172646

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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.