ArticlePloS one2014
Confirmation of childhood acute lymphoblastic leukemia variants, ARID5B and IKZF1, and interaction with parental environmental exposures.
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.
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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.
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.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- ARID5B gene polymorphisms and the risk of childhood acute lymphoblastic leukemia: a meta-analysis.International journal of hematology · 2019Pooled it
- Variants in ARID5B gene are associated with the development of acute lymphoblastic leukemia in Mexican children.Annals of hematology · 2019Trial
- Leukemia risk factor ARID5B coordinates HDAC-mediated transcriptional repression.Nucleic acids research · 2026Article
- Association Between Petroleum Compounds Exposure and Risk of Childhood Leukemia: A Systematic Review.Blood and lymphatic cancer : targets and therapy · 2026Review
- Predictive biosignatures for hospitalization in patients with virologically confirmed COVID-19.Journal of the Chinese Medical Association : JCMA · 2025Article
- Multi-step gene set analysis identified HTR3 family genes involving childhood acute lymphoblastic leukemia susceptibility.Archives of toxicology · 2025Article
- 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 · 2023Article
- Article
- Interaction between birth characteristics andFrontiers in oncology · 2023Article
- Molecular Mechanisms of ARID5B-Mediated Genetic Susceptibility to Acute Lymphoblastic Leukemia.Journal of the National Cancer Institute · 2022Article
- Diet as a Potential Moderator for Genome Stability and Immune Response in Pediatric Leukemia.Cancers · 2021Review
- Article
- Article
- Transcriptional Regulation of Genes by Ikaros Tumor Suppressor in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2020Review
- The Role of ARID5B in Acute Lymphoblastic Leukemia and Beyond.Frontiers in genetics · 2020Review
- IKZF1 genetic variants rs4132601 and rs11978267 and acute lymphoblastic leukemia risk in Tunisian children: a case-control study.BMC medical genetics · 2019Article
- 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 · 2019Review
- Aberrant ARID5B expression and its association with Ikaros dysfunction in acute lymphoblastic leukemia.Oncogenesis · 2018Article
- Primary Immunodeficiency and Cancer Predisposition Revisited: Embedding Two Closely Related Concepts Into an Integrative Conceptual Framework.Frontiers in immunology · 2018Review
- Genetic association with B-cell acute lymphoblastic leukemia in allogeneic transplant patients differs by age and sex.Blood advances · 2017Article
Corrections and comments
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Authors and funding
17 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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