Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia.

Vijayakrishnan, J; Studd, JORCID logo; Broderick, PORCID logo; Kinnersley, BORCID logo; Holroyd, A; Law, PJORCID logo; Kumar, R; Allan, JM; Harrison, CJ; Moorman, AV; +30 more...Vora, A; Roman, E; Rachakonda, S; Kinsey, SE; Sheridan, E; Thompson, PD; Irving, JA; Koehler, R; Hoffmann, P; Nöthen, MM; Heilmann-Heimbach, S; Jöckel, K; Easton, DFORCID logo; Pharaoh, PDORCID logo; Dunning, AM; Peto, JORCID logo; Canzian, FORCID logo; Swerdlow, A; Eeles, RAORCID logo; Kote-Jarai, Z; Muir, KORCID logo; Pashayan, NORCID logo; PRACTICAL Consortium; Greaves, M; Zimmerman, M; Bartram, CR; Schrappe, M; Stanulla, M; Hemminki, K; Houlston, RS and (2018) Genome-wide association study identifies susceptibility loci for B-cell childhood acute lymphoblastic leukemia. Nature communications, 9 (1). 1340-. ISSN 2041-1723 DOI: 10.1038/s41467-018-03178-z
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Genome-wide association studies (GWAS) have advanced our understanding of susceptibility to B-cell precursor acute lymphoblastic leukemia (BCP-ALL); however, much of the heritable risk remains unidentified. Here, we perform a GWAS and conduct a meta-analysis with two existing GWAS, totaling 2442 cases and 14,609 controls. We identify risk loci for BCP-ALL at 8q24.21 (rs28665337, P = 3.86 × 10-9, odds ratio (OR) = 1.34) and for ETV6-RUNX1 fusion-positive BCP-ALL at 2q22.3 (rs17481869, P = 3.20 × 10-8, OR = 2.14). Our findings provide further insights into genetic susceptibility to ALL and its biology.


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