Evidence map›Paper›PMID 30283812›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2018

Mononuclear cell transcriptome changes associated with dimethyl fumarate in MS.

Arie R Gafson, Kicheol Kim, Maria T Cencioni, Wim van Hecke, Richard Nicholas, Sergio E Baranzini, Paul M Matthews

Registry-linked trialOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04550455 (A Prospective Biomarker Study in Active Secondary Progressive Multiple Sclerosis), which is not on this map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 34% 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.

NCT04550455 phase4unknown statusnot on this mapstarted 2020, after this paper: background citation

A Prospective Biomarker Study in Active Secondary Progressive Multiple Sclerosis (SPMS)Subjects Treated With Cladribine Tablets

TypeinterventionalSponsorKeith Edwards, M.D.Ran2020 to 2025Enrolled30ConditionsMultiple SclerosisArmsCladribine Tablets
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

7 authors at 3 institutions in 3 countries.

Arie R GafsonDivision of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.
Kicheol KimDivision of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.
Maria T CencioniDivision of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.
Wim van HeckeDivision of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.
Richard NicholasDivision of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.
Sergio E BaranziniDivision of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.
Paul M MatthewsDivision of Brain Sciences (A.R.G., M.T.C., R.N.), Department of Medicine, Imperial College London; the Department of Neurology (K.K.), Weill Institute for Neurosciences, University of California, San Francisco; icometrix (W.v.H.), Begaultlaan, Leuven, Belgium; the Department of Neurology (S.E.B.), Weill Institute for Neurosciences, Institute for Human Genetics and Graduate Program in Bioinformatics, University of California, San Francisco; and Division of Brain Sciences (P.M.M.), Department of Medicine, the Centre for Neurotechnology and the UK Dementia Research Institute, Imperial College London.
Icometrix (Belgium) · BEUniversity of California, San Francisco · USImperial College London · GB

Funding

Medical Research Council G0900897Medical Research Council G9409531Medical Research Council G9409634Medical Research Council G9901399Medical Research Council MC_PC_17114Medical Research Council MR/K501013/1Medical Research Council MR/N026934/1Wellcome Trust
6 · The paper itself

Abstract

objectiveTo identify short-term changes in gene expression in peripheral blood mononuclear cells (PBMCs) associated with treatment response to dimethyl fumarate (DMF, Tecfidera) in patients with relapsing-remitting MS (RRMS).

methodsBlood samples were collected from 24 patients with RRMS (median Expanded Disability Status Scale score, 2.0; range 1-7) at baseline, 6 weeks, and 15 months after the initiation of treatment with DMF (BG-12; Tecfidera). Seven healthy controls were also recruited, and blood samples were collected over the same time intervals. PBMCs were extracted from blood samples and sequenced using next-generation RNA sequencing. Treatment responders were defined using the composite outcome measure "no evidence of disease activity" (NEDA-4). Time-course and cross-sectional differential expression analyses were performed to identify transcriptomic markers of treatment response.

resultsTreatment responders (NEDA-4 positive, 8/24) over the 15-month period had 478 differentially expressed genes (DEGs) 6 weeks after the start of treatment. These were enriched for nuclear factor (erythroid-derived 2)-like 2 (

conclusionShort-term PBMC transcriptome changes reflecting activation of the Nrf2 and inhibition of NFκB pathways distinguish patients who subsequently show a medium-term treatment response with DMF. Relative stabilization of gene expression patterns may accompany treatment-associated suppression of disease activity.

Identifiers

PMID30283812
PMCPMC6168332
OpenAlexW2808179851

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Registered trials

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.