Genome-wide association study identifies susceptibility loci for acute myeloid leukemia
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Lin, Wei-Yu | Fordham, Sarah | Hungate, Eric | Sunter, Nicola | Elstob, Claire | Xu, Yaobo | Park, Catherine | Quante, Anne | Strauch, Konstantin | Gieger, Christian | Skol, Andrew | Rahman, Thahira | Sucheston-Campbell, Lara | Wang, Junke | Hahn, Theresa | Clay-Gilmour, Alyssa | Jones, Gail | Marr, Helen | Jackson, Graham | Menne, Tobias | Collin, Mathew | Ivey, Adam | Hills, Robert | Burnett, Alan | Russell, Nigel | Fitzgibbon, Jude | Larson, Richard | Le Beau, Michelle | Stock, Wendy | Heidenreich, Olaf | Alharbi, Abrar | Allsup, David | Houlston, Richard | Norden, Jean | Dickinson, Anne | Douglas, Elisabeth | Lendrem, Clare | Daly, Ann | Palm, Louise | Piechocki, Kim | Jeffries, Sally | Bornhäuser, Martin | Röllig, Christoph | Altmann, Heidi | Ruhnke, Leo | Kunadt, Desiree | Wagenführ, Lisa | Cordell, Heather | Darlay, Rebecca | Andersen, Mette | Fontana, Maria | Martinelli, Giovanni | Marconi, Giovanni | Sanz, Miguel | Cervera, José | Gómez-Seguí, Inés | Cluzeau, Thomas | Moreilhon, Chimène | Raynaud, Sophie | Sill, Heinz | Voso, Maria Teresa | Lo-Coco, Francesco | Dombret, Hervé | Cheok, Meyling | Preudhomme, Claude | Gale, Rosemary | Linch, David | Gaal-Wesinger, Julia | Masszi, Andras | Nowak, Daniel | Hofmann, Wolf-Karsten | Gilkes, Amanda | Porkka, Kimmo | Milosevic Feenstra, Jelena | Kralovics, Robert | Grimwade, David | Meggendorfer, Manja | Haferlach, Torsten | Krizsán, Szilvia | Bödör, Csaba | Stölzel, Friedrich | Onel, Kenan | Allan, James
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Abstract Acute myeloid leukemia (AML) is a hematological malignancy with an undefined heritable risk. Here we perform a meta-analysis of three genome-wide association studies, with replication in a fourth study, incorporating a total of 4018 AML cases and 10488 controls. We identify a genome-wide significant risk locus for AML at 11q13.2 (rs4930561; P = 2.15 × 10 −8 ; KMT5B ). We also identify a genome-wide significant risk locus for the cytogenetically normal AML sub-group (N = 1287) at 6p21.32 (rs3916765; P = 1.51 × 10 −10 ; HLA ). Our results inform on AML etiology and identify putative functional genes operating in histone methylation ( KMT5B ) and immune function ( HLA ).
