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

Jayaram Vijayakrishnan, James Studd, Peter Broderick, Ben Kinnersley, Amy Holroyd, Philip J. Law, Rajiv Kumar, James M. Allan, Christine J. Harrison, Anthony V. Moorman, Ajay Vora, Eve Roman, Sivaramakrishna Rachakonda, Sally E. Kinsey, Eamonn Sheridan, Pamela D. Thompson, Julie A. Irving, Rolf Koehler, Per Hoffmann, Markus M. NöthenStefanie Heilmann-Heimbach, Karl Heinz Jöckel, Douglas F. Easton, Paul D.P. Pharaoh, Alison M. Dunning, Julian Peto, Frederico Canzian, Anthony Swerdlow, Rosalind A. Eeles, ZSofia Kote-Jarai, Kenneth Muir, Nora Pashayan, Mel Greaves, Martin Zimmerman, Claus R. Bartram, Martin Schrappe, Martin Stanulla, Kari Hemminki, Richard S. Houlston*, Brian E. Henderson, Christopher A. Haiman, Sara Benlloch, Fredrick R. Schumacher, Ali Amin Al Olama, Sonja I. Berndt, David V. Conti, Fredrik Wiklund, Stephen Chanock, Victoria L. Stevens, Børge G. Nordestgaard, The Practical Consortium

*Corresponding author af dette arbejde
28 Citationer (Scopus)
38 Downloads (Pure)

Abstract

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.

OriginalsprogEngelsk
Artikelnummer1340
TidsskriftNature Communications
Vol/bind9
Udgave nummer1
Antal sider14
ISSN2041-1723
DOI
StatusUdgivet - 2018

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