Genome-wide association study identifies susceptibility loci for acute myeloid leukemia.
- Lin, W-Y
- Fordham, SE
- Hungate, E
- Sunter, NJ
- Elstob, C
- Xu, Y
- Park, C
- Quante, A
- Strauch, K
- Gieger, C
- Skol, A
- Rahman, T
- Sucheston-Campbell, L
- Wang, J
- Hahn, T
- Clay-Gilmour, AI
- Jones, GL
- Marr, HJ
- Jackson, GH
- Menne, T
- Collin, M
- Ivey, A
- Hills, RK
- Burnett, AK
- Russell, NH
- Fitzgibbon, J
- Larson, RA
- Le Beau, MM
- Stock, W
- Heidenreich, O
- Alharbi, A
- Allsup, DJ
- Houlston, RS
- Norden, J
- Dickinson, AM
- Douglas, E
- Lendrem, C
- Daly, AK
- Palm, L
- Piechocki, K
- Jeffries, S
- Bornhäuser, M
- Röllig, C
- Altmann, H
- Ruhnke, L
- Kunadt, D
- Wagenführ, L
- Cordell, HJ
- Darlay, R
- Andersen, MK
- Fontana, MC
- Martinelli, G
- Marconi, G
- Sanz, MA
- Cervera, J
- Gómez-Seguí, I
- Cluzeau, T
- Moreilhon, C
- Raynaud, S
- Sill, H
- Voso, MT
- Lo-Coco, F
- Dombret, H
- Cheok, M
- Preudhomme, C
- Gale, RE
- Linch, D
- Gaal-Wesinger, J
- Masszi, A
- Nowak, D
- Hofmann, W-K
- Gilkes, A
- Porkka, K
- Milosevic Feenstra, JD
- Kralovics, R
- Grimwade, D
- Meggendorfer, M
- Haferlach, T
- Krizsán, S
- Bödör, C
- Stölzel, F
- Onel, K
- Allan, JM
Publication date
October 2021
DOI Publisher
Springer Science and Business Media LLC Journal
Nature CommunicationsAbstract
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)
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