Evidence map›Paper›PMID 19565504›Full record

ArticleArthritis and rheumatism2009

Gene expression signatures in polyarticular juvenile idiopathic arthritis demonstrate disease heterogeneity and offer a molecular classification of disease subsets.

Thomas A Griffin, Michael G Barnes, Norman T Ilowite, Judyann C Olson, David D Sherry, Beth S Gottlieb, Bruce J Aronow, Paul Pavlidis, Claas H Hinze, Sherry Thornton and 4 more

Abstract read
In one paragraph

Article in Arthritis and rheumatism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  17. A Novel Method for Pathway Identification Based on Attractor and Crosstalk in Polyarticular Juvenile Idiopathic Arthritis.Medical science monitor : international medical journal of experimental and clinical research · 2016
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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

14 authors.

Thomas A GriffinWilliam S. Rowe Division of Pediatric Rheumatology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. grift0@cchmc.org
Michael G Barnes
Norman T Ilowite
Judyann C Olson
David D Sherry
Beth S Gottlieb
Bruce J Aronow
Paul Pavlidis
Claas H Hinze
Sherry Thornton
Susan D Thompson
Alexei A Grom
Robert A Colbert
David N Glass

Funding

Pathogenic Mechanisms in SpondyloarthritisZIAAR041184 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$47.6M
Pediatric Rheumatology Tissue RepostoryP01AR048929 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI THOMPSON, SUSAN D · 2003 to 2015
$13.6M
PHARMACOGENOMICS OF JUVENILE RHEUMATOID ARTHRITISP60AR047784 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI LOVELL, DANIEL JOE · 2001 to 2012
$10.5M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI FLICK, MATTHEW J. · 2001 to 2015
$9.2M
NIAMS NIH HHS P01 AR048929NIAMS NIH HHS P01-AR-048929NIAMS NIH HHS P30-AR-47363NIAMS NIH HHS P60 AR047784NIAMS NIH HHS P60-AR-47784
6 · The paper itself

Abstract

objectiveTo determine whether peripheral blood mononuclear cells (PBMCs) from children with recent-onset polyarticular juvenile idiopathic arthritis (JIA) exhibit biologically or clinically informative gene expression signatures.

methodsPeripheral blood samples were obtained from 59 healthy children and 61 children with polyarticular JIA prior to treatment with second-line medications, such as methotrexate or biologic agents. RNA was extracted from isolated mononuclear cells, fluorescence labeled, and hybridized to commercial gene expression microarrays (Affymetrix HG-U133 Plus 2.0). Data were analyzed using analysis of variance at a 5% false discovery rate threshold after robust multichip analysis preprocessing and distance-weighted discrimination normalization.

resultsInitial analysis revealed 873 probe sets for genes that were differentially expressed between polyarticular JIA patients and healthy controls. Hierarchical clustering of these probe sets distinguished 3 subgroups within the polyarticular JIA group. Prototypical patients within each subgroup were identified and used to define subgroup-specific gene expression signatures. One of these signatures was associated with monocyte markers, another with transforming growth factor beta-inducible genes, and a third with immediate early genes. Correlation of gene expression signatures with clinical and biologic features of JIA subgroups suggested relevance to aspects of disease activity and supported the division of polyarticular JIA into distinct subsets.

conclusionGene expression signatures in PBMCs from patients with recent-onset polyarticular JIA reflect discrete disease processes and offer a molecular classification of disease.

Indexed as

Gene Expression ProfilingAdolescentAntibodies, AntinuclearAntirheumatic AgentsArthritisArthritis, JuvenileCase-Control StudiesChildChild, PreschoolFemaleGenes, Immediate-EarlyHumansLeukocytes, MononuclearMaleMethotrexateMultigene FamilyAntibodies, AntinuclearAntirheumatic AgentsMethotrexateRheumatoid FactorTransforming Growth Factor beta

Identifiers

PMID19565504
PMCPMC2741130

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Registered trials

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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.