ArticlePloS one2015
ARID5B, IKZF1 and non-genetic factors in the etiology of childhood acute lymphoblastic leukemia: the ESCALE study.
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 12 papers.
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12 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- The IKAROS Transcription Factor Gene IKZF1 as a Critical Regulator in the Pathogenesis of Childhood Acute Lymphoblastic Leukemia: Insights from a Bangladeshi Population.Indian journal of clinical biochemistry : IJCB · 2025Article
- Investigating the Impact of LNA-anti-miR-92b, miR-181b, TNF-α, and Piperine on Gene Expression and Cell Viability in Jurkat Cells: Implications for Acute Lymphoblastic Leukemia : LNA-anti- MicroRNAs and Jurkat Cells.Galen medical journal · 2025Article
- Genes of Predisposition to Childhood Beta-Cell Acute Lymphoblastic Leukemia in the Kazakh Population.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Transcriptomic Analysis of Conserved Telomere Maintenance Component 1 (CTC1) and Its Association with Leukemia.Journal of clinical medicine · 2022Article
- Association between maternal breastfeeding and risk of systemic neoplasms of offspring.Italian journal of pediatrics · 2022Review
- Acute lymphoid leukemia etiopathogenesis.Molecular biology reports · 2021Review
- Transcriptional Regulation of Genes by Ikaros Tumor Suppressor in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2020Review
- IKZF1 genetic variants rs4132601 and rs11978267 and acute lymphoblastic leukemia risk in Tunisian children: a case-control study.BMC medical genetics · 2019Article
- Aberrant ARID5B expression and its association with Ikaros dysfunction in acute lymphoblastic leukemia.Oncogenesis · 2018Article
- A causal mechanism for childhood acute lymphoblastic leukaemia.Nature reviews. Cancer · 2018Review
- IKZF1 gene polymorphisms increased the risk of childhood acute lymphoblastic leukemia in an Iranian population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
16 authors at 14 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) have identified that frequent polymorphisms in ARID5B and IKZF1, two genes involved in lymphoid differentiation, increase the risk of childhood acute lymphoblastic leukemia (ALL). These findings markedly modified the current field of research on the etiology of ALL. In this new context, the present exploratory study investigated the possible interactions between these at-risk alleles and the non-genetic suspected ALL risk factors that were of sufficient prevalence in the French ESCALE study: maternal use of home insecticides during pregnancy, preconception paternal smoking, and some proxies for early immune modulation, i.e. breastfeeding, history of common infections before age one year, and birth order. The analyses were based on 434 ALL cases and 442 controls of European origin, drawn from the nationwide population-based case-control study ESCALE. Information on non-genetic factors was obtained by standardized telephone interview. Interactions between rs10740055 in ARID5B or rs4132601 in IKZF1 and each of the suspected non-genetic factors were tested, with the SNPs coded as counts of minor alleles (trend variable). Statistical interactions were observed between rs4132601 and maternal insecticide use (p = 0.012), breastfeeding p = 0.017) and repeated early common infections (p = 0.0070), with allelic odds ratios (OR) which were only increased among the children not exposed to insecticides (OR = 1.8, 95%CI: 1.3, 2.4), those who had been breastfed (OR = 1.8, 95%CI: 1.3, 2.5) and those who had had repeated early common infections (OR = 2.4, 95%CI: 1.5, 3.8). The allelic ORs were close to one among children exposed to insecticides, who had not been breastfed and who had had no or few common infections. Repeated early common infections interacted with rs10740055 (p = 0.018) in the case-only design. Further studies are needed to evaluate whether these observations of a modification of the effect of the at-risk alleles by non-genetic factors are chance findings or reflect true underlying mechanisms.
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