Evidence map›Paper›PMID 25310577›Full record

ArticlePloS one2014

Confirmation of childhood acute lymphoblastic leukemia variants, ARID5B and IKZF1, and interaction with parental environmental exposures.

Tiffany-Jane Evans, Elizabeth Milne, Denise Anderson, Nicholas H de Klerk, Sarra E Jamieson, Bente A Talseth-Palmer, Nikola A Bowden, Elizabeth G Holliday, Jérémie Rudant, Laurent Orsi and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Review
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  7. Gene-Environment Analyses Reveal Novel Genetic Candidates with Prenatal Tobacco Exposure in Relation to Risk for Childhood Acute Lymphoblastic Leukemia.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023
    Article
  8. Haematologica · 2023
    Article
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  17. Is There Etiologic Heterogeneity between Subtypes of Childhood Acute Lymphoblastic Leukemia? A Review of Variation in Risk by Subtype.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    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

17 authors at 9 institutions in 2 countries.

Tiffany-Jane EvansCentre for Bioinformatics, Biomarker Discovery and Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
Elizabeth MilneTelethon Kids Institute, The University of Western Australia, Perth, Western Australia, Australia.
Denise AndersonTelethon Kids Institute, The University of Western Australia, Perth, Western Australia, Australia.
Nicholas H de KlerkTelethon Kids Institute, The University of Western Australia, Perth, Western Australia, Australia.
Sarra E JamiesonTelethon Kids Institute, The University of Western Australia, Perth, Western Australia, Australia.
Bente A Talseth-PalmerCentre for Bioinformatics, Biomarker Discovery and Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
Nikola A BowdenCentre for Bioinformatics, Biomarker Discovery and Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
Elizabeth G HollidayCentre for Bioinformatics, Biomarker Discovery and Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; Centre for Clinical Epidemiology and Biostatistics, School of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia.
Jérémie RudantINSERM, U1018, Department of Environmental Epidemiology of Cancers, Villejuif, France; Paris-Sud University, UMR-S1018, Department of Environmental Epidemiology of Cancers, Research Center in Epidemiology and Population Health, Villejuif, France.
Laurent OrsiINSERM, U1018, Department of Environmental Epidemiology of Cancers, Villejuif, France; Paris-Sud University, UMR-S1018, Department of Environmental Epidemiology of Cancers, Research Center in Epidemiology and Population Health, Villejuif, France; French National Registry of Childhood Blood Malignancies (RNHE), Villejuif, France.
Ebony RichardsonSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
Laura LavisSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia.
Daniel CatchpooleThe Tumour Bank, The Children's Cancer Research Unit, The Children's Hospital Westmead, Westmead, New South Wales, Australia.
John R AttiaCentre for Bioinformatics, Biomarker Discovery and Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; Centre for Clinical Epidemiology and Biostatistics, School of Medicine and Public Health, University of Newcastle, Newcastle, New South Wales, Australia; Department of Medicine, John Hunter Hospital and Hunter Medical Research Institute, New Lambton, New South Wales, Australia.
Bruce K ArmstrongSchool of Public Health, The University of Sydney and Sax Institute, Sydney, New South Wales, Australia.
Jacqueline ClavelINSERM, U1018, Department of Environmental Epidemiology of Cancers, Villejuif, France; Paris-Sud University, UMR-S1018, Department of Environmental Epidemiology of Cancers, Research Center in Epidemiology and Population Health, Villejuif, France; French National Registry of Childhood Blood Malignancies (RNHE), Villejuif, France.
Rodney J ScottCentre for Bioinformatics, Biomarker Discovery and Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia; School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, New South Wales, Australia; Molecular Genetics, Hunter Area Pathology Service, Newcastle, New South Wales, Australia.
University of Newcastle Australia · AUUniversity of Western Australia · AUHunter Medical Research Institute · AUUniversité Paris-Sud · FRCentre de recherche en Epidémiologie et Santé des Populations · FRChildren's Hospital at Westmead · AUJohn Hunter Hospital · AUThe Kids Research Institute Australia · AUUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome wide association studies (GWAS) have established association of ARID5B and IKZF1 variants with childhood acute lymphoblastic leukemia (ALL). Epidemiological studies suggest that environmental factors alone appear to make a relatively minor contribution to disease risk. The polygenic nature of childhood ALL predisposition together with the timing of environmental triggers may hold vital clues for disease etiology. This study presents results from an Australian GWAS of childhood ALL cases (n = 358) and population controls (n = 1192). Furthermore, we utilised family trio (n = 204) genotypes to extend our investigation to gene-environment interaction of significant loci with parental exposures before conception, and child's sex and age. Thirteen SNPs achieved genome wide significance in the population based case/control analysis; ten annotated to ARID5B and three to IKZF1. The most significant SNPs in these regions were ARID5B rs4245595 (OR 1.63, CI 1.38-1.93, P = 2.13×10(-9)), and IKZF1 rs1110701 (OR 1.69, CI 1.42-2.02, p = 7.26×10(-9)). There was evidence of gene-environment interaction for risk genotype at IKZF1, whereby an apparently stronger genetic effect was observed if the mother took folic acid or if the father did not smoke prior to pregnancy (respective interaction P-values: 0.04, 0.05). There were no interactions of risk genotypes with age or sex (P-values >0.2). Our results evidence that interaction of genetic variants and environmental exposures may further alter risk of childhood ALL however, investigation in a larger population is required. If interaction of folic acid supplementation and IKZF1 variants holds, it may be useful to quantify folate levels prior to initiating use of folic acid supplements.

Indexed as

Environmental ExposureGene-Environment InteractionParentsAdultChildDNA-Binding ProteinsFemaleGenome-Wide Association StudyHumansIkaros Transcription FactorMalePolymorphism, Single NucleotidePrecursor Cell Lymphoblastic Leukemia-LymphomaReproducibility of ResultsTranscription FactorsARID5B protein, humanDNA-Binding ProteinsIkaros Transcription FactorIKZF1 protein, humanTranscription Factors

Identifiers

PMID25310577
PMCPMC4195717
OpenAlexW2047677299

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.