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Vijayakrishnan, Jayaram; Qian, Maoxiang; Studd, James B; Yang, Wenjian; Kinnersley, Ben; Law, Philip J; Broderick, Peter; Raetz, Elizabeth A; Allan, James; Pui, Ching-Hon; Vora, Ajay; Evans, William E; Moorman, Anthony; Yeoh, Allen; Yang, Wentao; Li, Chunliang; Bartram, Claus R; Mullighan, Charles G; Zimmerman, Martin; Hunger, Stephen P; Schrappe, Martin; Relling, Mary V; Stanulla, Martin; Loh, Mignon L; Houlston, Richard S; Yang, Jun J
Nature communications, 11/2019, Letnik: 10, Številka: 1Journal Article
There is increasing evidence for a strong inherited genetic basis of susceptibility to acute lymphoblastic leukaemia (ALL) in children. To identify new risk variants for B-cell ALL (B-ALL) we conducted a meta-analysis with four GWAS (genome-wide association studies), totalling 5321 cases and 16,666 controls of European descent. We herein describe novel risk loci for B-ALL at 9q21.31 (rs76925697, P = 2.11 × 10 ), for high-hyperdiploid ALL at 5q31.1 (rs886285, P = 1.56 × 10 ) and 6p21.31 (rs210143 in BAK1, P = 2.21 × 10 ), and ETV6-RUNX1 ALL at 17q21.32 (rs10853104 in IGF2BP1, P = 1.82 × 10 ). Particularly notable are the pleiotropic effects of the BAK1 variant on multiple haematological malignancies and specific effects of IGF2BP1 on ETV6-RUNX1 ALL evidenced by both germline and somatic genomic analyses. Integration of GWAS signals with transcriptomic/epigenomic profiling and 3D chromatin interaction data for these leukaemia risk loci suggests deregulation of B-cell development and the cell cycle as central mechanisms governing genetic susceptibility to ALL.
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in: SICRIS
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