Evidence map›Paper›PMID 23019656›Full record

ArticleScience translational medicine2012

An RNA profile identifies two subsets of multiple sclerosis patients differing in disease activity.

Linda Ottoboni, Brendan T Keenan, Pablo Tamayo, Manik Kuchroo, Jill P Mesirov, Guy J Buckle, Samia J Khoury, David A Hafler, Howard L Weiner, Philip L De Jager

Open access · greenAbstract read
In one paragraph

Article in Science translational medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. The molecular subtypes of autoimmune diseases.Computational and structural biotechnology journal · 2024
    Review
  7. Pathogenic autoantibody internalization in myositis.medRxiv : the preprint server for health sciences · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. A pathogenic and clonally expanded B cell transcriptome in active multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. MSNeurology(R) neuroimmunology & neuroinflammation · 2018
    Article
  17. Article
  18. Review
  19. Blood Biomarkers as Outcome Measures in Inflammatory Neurologic Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
  20. Multiple sclerosis: genetics, biomarkers, treatments.Current opinion in neurology · 2016
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Linda OttoboniProgram in Translational Neuropsychiatric Genomics, Institute for the Neurosciences, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02115, USA.
Brendan T Keenan
Pablo Tamayo
Manik Kuchroo
Jill P Mesirov
Guy J Buckle
Samia J Khoury
David A Hafler
Howard L Weiner
Philip L De Jager
Broad Institute · USHarvard University · US

Funding

Role of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI David A. Hafler · 1996 to 2026
$51.7M
ACE: Investigation of Innate Immunity in Multiple SclerosisR01AI091568 · NIAID · YALE UNIVERSITY · PI HAFLER, DAVID A. · 2010 to 2014
$1.6M
Exploring the consequences of the TNFRSF1A susceptibility allele for MSR01NS067305 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI DE JAGER, PHILIP L · 2009 to 2011
$1.2M
NIAID NIH HHS P01 AI039671NIAID NIH HHS R01 AI091568NINDS NIH HHS R01 NS067305
6 · The paper itself

Abstract

The multiple sclerosis (MS) patient population is highly heterogeneous in terms of disease course and treatment response. We used a transcriptional profile generated from peripheral blood mononuclear cells to define the structure of an MS patient population. Two subsets of MS subjects (MS(A) and MS(B)) were found among 141 untreated subjects. We replicated this structure in two additional groups of MS subjects treated with one of the two first-line disease-modifying treatments in MS: glatiramer acetate (GA) (n = 94) and interferon-β (IFN-β) (n = 128). One of the two subsets of subjects (MS(A)) was distinguished by higher expression of molecules involved in lymphocyte signaling pathways. Further, subjects in this MS(A) subset were more likely to have a new inflammatory event while on treatment with either GA or IFN-β (P = 0.0077). We thus report a transcriptional signature that differentiates subjects with MS into two classes with different levels of disease activity.

Indexed as

Gene Expression ProfilingAdultCluster AnalysisDemographyDemyelinating DiseasesDisease ProgressionFemaleGlatiramer AcetateHumansInterferon-betaLikelihood FunctionsMaleMolecular Sequence AnnotationMultiple SclerosisPeptidesRNAGlatiramer AcetateInterferon-betaPeptidesRNA

Identifiers

PMID23019656
PMCPMC3753678
OpenAlexW2143735963

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.