Evidence map›Paper›PMID 26457809›Full record

ArticlePloS one2015

Subgroups of Paediatric Acute Lymphoblastic Leukaemia Might Differ Significantly in Genetic Predisposition to Asparaginase Hypersensitivity.

Nóra Kutszegi, Ágnes F Semsei, András Gézsi, Judit C Sági, Viktória Nagy, Katalin Csordás, Zsuzsanna Jakab, Orsolya Lautner-Csorba, Krisztina Míta Gábor, Gábor T Kovács and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Evaluating the Frequencies ofThe application of clinical genetics · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Pharmacogenetics of asparaginase in acute lymphoblastic leukemia.Cancer drug resistance (Alhambra, Calif.) · 2019
    Review
  10. Article
  11. Review
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

12 authors at 2 institutions in 1 country.

Nóra KutszegiDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Ágnes F SemseiDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
András GézsiDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Judit C SágiDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Viktória Nagy2nd Department of Paediatrics, Semmelweis University, Budapest, Hungary.
Katalin Csordás2nd Department of Paediatrics, Semmelweis University, Budapest, Hungary.
Zsuzsanna Jakab2nd Department of Paediatrics, Semmelweis University, Budapest, Hungary.
Orsolya Lautner-CsorbaDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Krisztina Míta GáborDepartment of Pediatrics and Pediatric Health Care Center, Faculty of Medicine, University of Szeged, Szeged, Hungary.
Gábor T Kovács2nd Department of Paediatrics, Semmelweis University, Budapest, Hungary.
Dániel J Erdélyi2nd Department of Paediatrics, Semmelweis University, Budapest, Hungary.
Csaba Szalai2nd Department of Paediatrics, Semmelweis University, Budapest, Hungary; Central Laboratory, Heim Pal Children Hospital, Budapest, Hungary.
Semmelweis University · HUUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

L-asparaginase (ASP) is a key element in the treatment of paediatric acute lymphoblastic leukaemia (ALL). However, hypersensitivity reactions (HSRs) to ASP are major challenges in paediatric patients. Our aim was to investigate genetic variants that may influence the risk to Escherichia coli-derived ASP hypersensitivity. Sample and clinical data collection was carried out from 576 paediatric ALL patients who were treated according to protocols from the Berlin-Frankfurt-Münster Study Group. A total of 20 single nucleotide polymorphisms (SNPs) in GRIA1 and GALNT10 genes were genotyped. Patients with GRIA1 rs4958351 AA/AG genotype showed significantly reduced risk to ASP hypersensitivity compared to patients with GG genotype in the T-cell ALL subgroup (OR = 0.05 (0.01-0.26); p = 4.70E-04), while no such association was found in pre-B-cell ALL. In the medium risk group two SNPs of GRIA1 (rs2055083 and rs707176) were associated significantly with the occurrence of ASP hypersensitivity (OR = 0.21 (0.09-0.53); p = 8.48E-04 and OR = 3.02 (1.36-6.73); p = 6.76E-03, respectively). Evaluating the genders separately, however, the association of rs707176 with ASP HSRs was confined only to females. Our results suggest that genetic variants of GRIA1 might influence the risk to ASP hypersensitivity, but subgroups of patients can differ significantly in this respect.

Indexed as

Genetic Predisposition to DiseaseAdolescentAllelesAntineoplastic AgentsAsparaginaseChildChild, PreschoolDrug HypersensitivityFemaleGenetic Association StudiesGenotypeHumansInfantMalePolymorphism, Single NucleotidePrecursor Cell Lymphoblastic Leukemia-LymphomaAntineoplastic AgentsAsparaginase

Identifiers

PMID26457809
PMCPMC4601692
OpenAlexW1898867566

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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.