Evidence map›Paper›PMID 23809696›Full record

ArticleGenome medicine2013

Peripheral blood derived gene panels predict response to infliximab in rheumatoid arthritis and Crohn's disease.

Bertalan Mesko, Szilard Poliska, Andrea Váncsa, Zoltan Szekanecz, Karoly Palatka, Zsolt Hollo, Attila Horvath, Laszlo Steiner, Gabor Zahuczky, Janos Podani and 1 more

Open access · goldAbstract read
In one paragraph

Article in Genome medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 3 pooled it
2.8field-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

29 citing papers in PubMed, 3 syntheses or guidelines pooled it, 49 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

11 authors at 4 institutions in 1 country.

Bertalan MeskoDepartment of Biochemistry and Molecular Biology, Debrecen, Egyetemtér, 4028, Hungary.
Szilard PoliskaDepartment of Biochemistry and Molecular Biology, Debrecen, Egyetemtér, 4028, Hungary ; Center for Clinical Genomics and Personalized Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Egyetemtér, 4028, Hungary ; UD-GenoMed, Ltd., Debrecen, Egyetemtér, 4012, Pf 52, Hungary.
Andrea VáncsaDepartment of Rheumatology, Institute of Medicine, University of Debrecen, Medical and Health Science Center, Debrecen, Egyetemtér, 4028, Hungary.
Zoltan SzekaneczDepartment of Rheumatology, Institute of Medicine, University of Debrecen, Medical and Health Science Center, Debrecen, Egyetemtér, 4028, Hungary.
Karoly Palatka2nd Department of Internal Medicine, University of Debrecen, Medical and Health Science Center, Debrecen, Egyetemtér, 4028, Hungary.
Zsolt HolloEGIS Pharmaceuticals, H-1106 Budapest, Keresztúriút 30-38, Hungary.
Attila HorvathCenter for Clinical Genomics and Personalized Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Egyetemtér, 4028, Hungary.
Laszlo SteinerCenter for Clinical Genomics and Personalized Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Egyetemtér, 4028, Hungary.
Gabor ZahuczkyUD-GenoMed, Ltd., Debrecen, Egyetemtér, 4012, Pf 52, Hungary.
Janos PodaniBiological Institute, LorandEötvös University, H-1117 Budapest, Egyetemtér, Hungary.
And Laszlo NagyDepartment of Biochemistry and Molecular Biology, Debrecen, Egyetemtér, 4028, Hungary ; MTA-DE "Lendulet" Immunogenomics Research Group, Research Center for Molecular Medicine, University of Debrecen, Medical and Health Science Center Debrecen,Egyetemtér, 4028, Hungary ; Center for Clinical Genomics and Personalized Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Egyetemtér, 4028, Hungary.
University of Debrecen · HUEgis Pharmaceuticals (Hungary) · HUEötvös Loránd University · HUUD-GenoMed (Hungary) · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBiological therapies have been introduced for the treatment of chronic inflammatory diseases including rheumatoid arthritis (RA) and Crohn's disease (CD). The efficacy of biologics differs from patient to patient. Moreover these therapies are rather expensive, therefore treatment of primary non-responders should be avoided.

methodWe addressed this issue by combining gene expression profiling and biostatistical approaches. We performed peripheral blood global gene expression profiling in order to filter the genome for target genes in cohorts of 20 CD and 19 RA patients. Then RT-quantitative PCR validation was performed, followed by multivariate analyses of genes in independent cohorts of 20 CD and 15 RA patients, in order to identify sets ofinterrelated genes that can separate responders from non-responders to the humanized chimeric anti-TNFalpha antibody infliximab at baseline.

resultsGene panels separating responders from non-responders were identified using leave-one-out cross-validation test, and a pool of genes that should be tested on larger cohorts was created in both conditions.

conclusionsOur data show that peripheral blood gene expression profiles are suitable for determining gene panels with high discriminatory power to differentiate responders from non-responders in infliximab therapy at baseline in CD and RA, which could be cross-validated successfully. Biostatistical analysis of peripheral blood gene expression data leads to the identification of gene panels that can help predict responsiveness of therapy and support the clinical decision-making process.

Identifiers

PMID23809696
PMCPMC4064310
OpenAlexW2160208009

What OpenQuestion holds

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LicenceCC BY
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.