Evidence map›Paper›PMID 25927497›Full record

SynthesisArthritis research & therapy2015

Anti-citrullinated peptide/protein antibody (ACPA)-negative RA shares a large proportion of susceptibility loci with ACPA-positive RA: a meta-analysis of genome-wide association study in a Japanese population.

Chikashi Terao, Koichiro Ohmura, Yuta Kochi, Katsunori Ikari, Yukinori Okada, Masakazu Shimizu, Naoshi Nishina, Akari Suzuki, Keiko Myouzen, Takahisa Kawaguchi and 22 more

Open access · goldAbstract readComparative StudyMeta-AnalysisReview
In one paragraph

Synthesis in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Fc receptor-like 1, 3, and 6 variants are associated with rheumatoid arthritis risk in the Chinese Han population.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Genetic landscape of interactive effects ofJournal of medical genetics · 2017
    Article
  12. Review
  13. Recent Advances in Defining the Genetic Basis of Rheumatoid Arthritis.Annual review of genomics and human genetics · 2016
    Review
  14. 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

32 authors at 11 institutions in 2 countries.

Chikashi TeraoCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. a0001101@kuhp.kyoto-u.ac.jp.
Koichiro OhmuraDepartment of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan. ohmurako@kuhp.kyoto-u.ac.jp.
Yuta KochiLaboratory for Autoimmune Diseases, Center for Genomic Medicine, RIKEN, Yokohama, Japan. ykochi@src.riken.jp.
Katsunori IkariInstitute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan. kikari@mac.com.
Yukinori OkadaDepartment of Human Genetics and Disease Diversity, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. yokada.brc@tmd.ac.jp.
Masakazu ShimizuCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. shimmy@kuhp.kyoto-u.ac.jp.
Naoshi NishinaDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. nnnmd11@hotmail.com.
Akari SuzukiLaboratory for Autoimmune Diseases, Center for Genomic Medicine, RIKEN, Yokohama, Japan. akaris@src.riken.jp.
Keiko MyouzenLaboratory for Autoimmune Diseases, Center for Genomic Medicine, RIKEN, Yokohama, Japan. keimyouzen@src.riken.jp.
Takahisa KawaguchiCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. tkawa@genome.med.kyoto-u.ac.jp.
Meiko TakahashiCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. meiko@genome.med.kyoto-u.ac.jp.
Kiyoshi TakasugiDohgo Spa Hospital, Matsuyama, Japan. keetakas@ehime.med.or.jp.
Akira MurasawaDepartment of Rheumatology, Niigata Rheumatic Center, Niigata, Japan. med@ra-center.com.
Shinichi MizukiThe Centre for Rheumatic Diseases, Matsuyama Red Cross Hospital, Matsuyama, Japan. smizuki@matsuyama.jrc.or.jp.
Mitsuhiro IwahashiHigashihiroshima Memorial Hospital, Hiroshima, Japan. ajisu@hotmail.com.
Keiko FunahashiPharm C, Matsubara Mayflower Hospital, 944-25 Fujita, Kato City, Hyogo, Japan. kansetsusaisei123@cup.ocn.ne.jp.
Masamitsu NatsumedaKurashiki Sweet Hospital, Kurashiki, Japan. zaraspook3hook@yahoo.co.jp.
Moritoshi FuruDepartment of the Control for Rheumatic Diseases, Kyoto University Graduate School of Medicine, Kyoto, Japan. morifuru@kuhp.kyoto-u.ac.jp.
Motomu HashimotoDepartment of the Control for Rheumatic Diseases, Kyoto University Graduate School of Medicine, Kyoto, Japan. mohashim@kuhp.kyoto-u.ac.jp.
Hiromu ItoDepartment of the Control for Rheumatic Diseases, Kyoto University Graduate School of Medicine, Kyoto, Japan. hiromu@kuhp.kyoto-u.ac.jp.
Takao FujiiDepartment of the Control for Rheumatic Diseases, Kyoto University Graduate School of Medicine, Kyoto, Japan. takfujii@kuhp.kyoto-u.ac.jp.
Kazuhiko EzawaKurashiki Sweet Hospital, Kurashiki, Japan. ky-6182@rice.ocn.ne.jp.
Tsukasa MatsubaraMatsubara Mayflower Hospital, 944-25 Fujita, Kato City, Hyogo, Japan. mats@mayflower-hp.jp.
Tsutomu TakeuchiDivision of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. tsutake@z5.keio.jp.
Michiaki KuboLaboratory for Autoimmune Diseases, Center for Genomic Medicine, RIKEN, Yokohama, Japan. mkubo@src.riken.jp.
Ryo YamadaCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. ryamada@genome.med.kyoto-u.ac.jp.
Atsuo TaniguchiInstitute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan. amtanigu@ior.twmu.ac.jp.
Hisashi YamanakaInstitute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan. yamanaka@ior.twmu.ac.jp.
Shigeki MomoharaInstitute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan. smomohara@ior.twmu.ac.jp.
Kazuhiko YamamotoLaboratory for Autoimmune Diseases, Center for Genomic Medicine, RIKEN, Yokohama, Japan. yamamoto-tky@umin.ac.jp.
Tsuneyo MimoriDepartment of Rheumatology and Clinical Immunology, Kyoto University Graduate School of Medicine, Kyoto, 606-8507, Japan. mimorit@kuhp.kyoto-u.ac.jp.
Fumihiko MatsudaCenter for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. fumi@genome.med.kyoto-u.ac.jp.
Kyoto University · JPRIKEN Center for Integrative Medical Sciences · JPTokyo Women's Medical University · JPKeio University · JPKurashiki Central Hospital · JPKyoto University of Education · JPMatsubara Mayflower Hospital · JPDogo Onsen Hospital · JPHigashihiroshima Medical Center · JPMatsuyama Red Cross Hospital · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAlthough susceptibility genes for anti-citrullinated peptide/protein antibodies (ACPA)-positive rheumatoid arthritis (RA) have been successfully discovered by genome-wide association studies (GWAS), little is known about the genetic background of ACPA-negative RA. We intended to elucidate genetic background of ACPA-negative RA.

methodWe performed a meta-analysis of GWAS comprising 670 ACPA-negative RA and 16,891 controls for 1,948,138 markers, followed by a replication study of the top 35 single nucleotide polymorphisms (SNPs) using 916 cases and 3,764 controls. Inverse-variance method was applied to assess overall effects. To assess overlap of susceptibility loci between ACPA-positive and -negative RA, odds ratios (ORs) of the 21 susceptibility markers to RA in Japanese were compared between the two subsets. In addition, SNPs were stratified by the p-values in GWAS meta-analysis for either ACPA-positive RA or ACPA-negative RA to address the question whether weakly-associated genes were also shared. The correlations between ACPA-positive RA and the subpopulations of ACPA-negative RA (rheumatoid factor (RF)-positive and RF-negative subsets) were also addressed.

resultsRs6904716 in LEMD2 of the human leukocyte antigen (HLA) locus showed a borderline association with ACPA-negative RA (overall p = 5.7 × 10(-8)), followed by rs6986423 in CSMD1 (p = 2.4 × 10(-6)) and rs17727339 in FCRL3 (p = 1.4 × 10(-5)). ACPA-negative RA showed significant correlations of ORs with ACPA-positive RA for the 21 susceptibility SNPs and non-HLA SNPs with p-values far from significance. These significant correlations with ACPA-positive RA were true for ACPA-negative RF-positive and ACPA-negative RF-negative RA. On the contrary, positive correlations were not observed between the ACPA-negative two subpopulations.

conclusionMany of the susceptibility loci were shared between ACPA-positive and -negative RA.

Indexed as

Genome-Wide Association StudyArthritis, RheumatoidAsian PeopleFemaleGenetic LociGenetic Predisposition to DiseaseGenotypeHumansJapanMalePeptides, CyclicPolymorphism, Single NucleotideReference Valuescyclic citrullinated peptidePeptides, Cyclic

Identifiers

PMID25927497
PMCPMC4431175
OpenAlexW2089920716

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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.