Evidence map›Paper›PMID 22763757›Full record

ArticleEuropean journal of clinical pharmacology2013

Association of the TYMS 3G/3G genotype with poor response and GGH 354GG genotype with the bone marrow toxicity of the methotrexate in RA patients.

Biljana Jekic, Ljiljana Lukovic, Vera Bunjevacki, Vera Milic, Ivana Novakovic, Tatjana Damnjanovic, Jelena Milasin, Branka Popovic, Nela Maksimovic, Nemanja Damjanov and 3 more

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In one paragraph

Article in European journal of clinical pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 5 pooled it
5.0field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 5 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Genetic markers in methotrexate treatments.The pharmacogenomics journal · 2018
    Pooled it
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  6. Pharmacogenetics of Drug Therapies in Rheumatoid Arthritis.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
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  16. Genetics as a molecular window into recovery, its treatment, and stress responses after stroke.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2016
    Review
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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

13 authors at 2 institutions in 2 countries.

Biljana JekicInstitute of Human Genetics, Faculty of Medicine, University of Belgrade, 26 Visegradska Str, 11000 Belgrade, Serbia. jekic.b@gmail.com
Ljiljana Lukovic
Vera Bunjevacki
Vera Milic
Ivana Novakovic
Tatjana Damnjanovic
Jelena Milasin
Branka Popovic
Nela Maksimovic
Nemanja Damjanov
Goran Radunovic
Ljiljana Kovacevic
Maja Krajinovic
University of Belgrade · RSCentre Hospitalier Universitaire Sainte-Justine · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGamma-glutamyl hydrolase (GGH), cyclin D1 (CCND1) and thymidylate synthase (TS) genes encode enzymes that are involved in methotrexate (MTX) action. In a group of 184 RA patients treated with MTX, we have investigated whether selected polymorphisms in these genes modulate MTX efficacy and/or have impact on adverse drug effects (ADEs).

methodsThe efficacy of the MTX therapy has been estimated using the disease activity score in 28 joints (DAS28-ESR) based on EULAR criteria and relative DAS28 values (rDAS28). All adverse drug events were recorded. Patients were genotyped for selected polymorphisms of the GGH (-354 G > T and 452 C > T), CCND1 (870 A > G) and TYMS (variable number of tandem repeats, VNTR, and G to C substitution of triple repeat, 3R allele) gene. Association studies have been performed between obtained genotypes and the efficacy and toxicity of MTX.

resultsAccording to the EULAR response criteria, 146 RA patients (79.3 %) were classified as responders (good/moderate response) and 38 (20.7 %) as non-responders (poor response). Higher frequency of the TYMS 3 G/3 G genotype has been found among non-responders as compared to individuals with remaining genotypes (p = 0.02). ADEs were recorded in 53 patients. Among those patients eight experienced bone marrow toxicity, all of them carried GGH -354GG genotype (p = 0.003). No other significant association were observed.

conclusionThe 3 G/3 G genotype of the TYMS gene may indicate predisposition of poor response to MTX and GG genotype of GGH -354 T > G polymorphism may have high predictive value for myelosuppression in RA patients.

Indexed as

Polymorphism, GeneticAdultAgedAged, 80 and overAnalysis of VarianceAntirheumatic AgentsArthritis, RheumatoidBone MarrowBone Marrow DiseasesChi-Square DistributionCyclin D1Femalegamma-Glutamyl HydrolaseGene FrequencyGenetic Predisposition to DiseaseHumansAntirheumatic AgentsCCND1 protein, humanCyclin D1gamma-Glutamyl HydrolaseMethotrexateThymidylate Synthase

Identifiers

PMID22763757
OpenAlexW2048702921

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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.