DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Acute lymphoblastic leukemia in childhood (B cell precursor). The EFO term B-cell acute lymphoblastic leukemia was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: B-cell acute lymphoblastic leukemia

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

J Vijayakrishnan, R Kumar, MY Henrion, AV Moorman, PS Rachakonda, I Hosen, MI da Silva Filho, A Holroyd, SE Dobbins, R Koehler, H Thomsen, JA Irving, JM Allan, T Lightfoot, E Roman, SE Kinsey, E Sheridan, PD Thompson, P Hoffmann, MM Nöthen, S Heilmann-Heimbach, KH Jöckel, M Greaves, CJ Harrison, CR Bartram, M Schrappe, M Stanulla, K Hemminki, RS Houlston

TITLE:

A genome-wide association study identifies risk loci for childhood acute lymphoblastic leukemia at 10q26.13 and 12q23.1.

JOURNAL:

Leukemia Mar 2017, Vol 31, pp. 573-579

ABSTRACT:

Genome-wide association studies (GWASs) have shown that common genetic variation contributes to the heritable risk of childhood acute lymphoblastic leukemia (ALL). To identify new susceptibility loci for the largest subtype of ALL, B-cell precursor ALL (BCP-ALL), we conducted a meta-analysis of two GWASs with imputation using 1000 Genomes and UK10K Project data as reference (totaling 1658 cases and 7224 controls). After genotyping an additional 2525 cases and 3575 controls, we identify new susceptibility loci for BCP-ALL mapping to 10q26.13 (rs35837782, LHPP, P=1.38 × 10(-11)) and 12q23.1 (rs4762284, ELK3, P=8.41 × 10(-9)). We also provide confirmatory evidence for the existence of independent risk loci at 9p21.3, but show that the association marked by rs77728904 can be accounted for by linkage disequilibrium with the rare high-impact CDKN2A p.Ala148Thr variant rs3731249. Our data provide further insights into genetic susceptibility to ALL and its biology. PUBMED: 27694927
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