Evidence map›Paper›PMID 41437385›Full record

ArticleHuman genomics2025

Identification of potential predictive biomarkers during JAK-inhibitor therapies in rheumatoid arthritis.

János Rózsa, Dóra Csige, Monika Bodoki, Zsófia Hagymási-Szabó, Ferenc Tóth, Szilvia Szamosi, Ágnes Horváth, Nóra Bodnár, Edit Végh, Sándor Szántó and 7 more

Abstract read
In one paragraph

Article in Human genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

17 authors.

János Rózsa *Genomic Medicine and Bioinformatics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Dóra Csige *Institute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Monika BodokiInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zsófia Hagymási-SzabóUD-GenoMed Medical Genomic Technologies Ltd, Debrecen, Hungary.
Ferenc TóthUD-GenoMed Medical Genomic Technologies Ltd, Debrecen, Hungary.
Szilvia SzamosiInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Ágnes HorváthInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Nóra BodnárInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Edit VéghInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Sándor SzántóInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Gabriella SzűcsInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zsófia PethőInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zsuzsanna GyetkóInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Levente BodokiInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
János KádasUD-GenoMed Medical Genomic Technologies Ltd, Debrecen, Hungary.
Zoltán SzekaneczInstitute of Internal Medicine, Department of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Szilárd PóliskaGenomic Medicine and Bioinformatics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. poliska@med.unideb.hu.

Funding

European Union GINOP-2.3.2-15-2016-00050Ministry for Culture and Innovation of Hun¬gary from the National Research, Development and Innovation Fund TKP2021-NKTA-34
6 · The paper itself

Abstract

backgroundTargeted synthetic therapeutics, such as Janus kinase (JAK) inhibitors, have opened up a new platform for the treatment of various diseases, including rheumatoid arthritis (RA). As with all drugs, the efficacy of different medicine may vary from patient to patient, and there may be different side effects if the expected effect is not achieved. In addition to the uncertain success of treatments, they also place a heavy burden on the health care system, making the identification of potential predictive biomarkers for drug optimisation highly valuable.

methodsIn order to identify potential predictive biomarkers, 28 patients with RA were recruited and blood samples were taken twice–before medical treatment and after 6 months of continuous therapy. Peripheral blood mononuclear cells (PBMCs) were isolated from blood samples and after RNA isolation, RNA sequencing was performed using high throughput sequencing technology to generate global gene expression data. Validation of target genes was conducted using real-time quantitative PCR methods.

resultsAfter data analyses we examined the gene expression changes between the two sampling time points and responder versus non-responder groups. 225 genes showed significantly different expression between T6 and T0 samples, while 60 and 66 genes showed differential expression between the responder and non-responder patients at T0 and T6 sampling points, respectively. 13 differentially expressed genes were common between two time points and showed the same direction in regulation.

conclusionsBased on our results, several RA-relevant genes were identified, as a result of the JAK-inhibitor treatments in comparison of T6 versus T0 samples. At both time points, the differentially expressed genes between responder and non-responder groups could separate the samples, however, the separation was not clear. The identified 13 common genes could also partially separate the responder and non-responder groups from each other. These sets of genes could be the source of potential biomarkers, which could help predict the responsiveness of patients to JAK inhibitor therapy.

Indexed as

Arthritis, RheumatoidBiomarkersJanus Kinase InhibitorsJanus KinasesAgedFemaleGene Expression ProfilingHumansLeukocytes, MononuclearMaleMiddle AgedPyrimidinesBiomarkersJanus Kinase InhibitorsJanus KinasesPyrimidinesGene expressionJAK inhibitorsJanus kinasePredictionResponseRheumatoid arthritisRNA-sequencing

Identifiers

PMID41437385
PMCPMC12837950

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.