Genome-wide association study identifies multiple susceptibility loci for multiple myeloma.
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Authors
Mitchell, Jonathan SLi, Ni
Weinhold, Niels
Försti, Asta
Ali, Mina
van Duin, Mark
Thorleifsson, Gudmar
Johnson, David C
Chen, Bowang
Halvarsson, Britt-Marie
Gudbjartsson, Daniel F
Kuiper, Rowan
Stephens, Owen W
Bertsch, Uta
Broderick, Peter
Campo, Chiara
Einsele, Hermann
Gregory, Walter A
Gullberg, Urban
Henrion, Marc
Hillengass, Jens
Hoffmann, Per
Jackson, Graham H
Johnsson, Ellinor
Jöud, Magnus
Kristinsson, Sigurður Y
Lenhoff, Stig
Lenive, Oleg
Mellqvist, Ulf-Henrik
Migliorini, Gabriele
Nahi, Hareth
Nelander, Sven
Nickel, Jolanta
Nöthen, Markus M
Rafnar, Thorunn
Ross, Fiona M
da Silva Filho, Miguel Inacio
Swaminathan, Bhairavi
Thomsen, Hauke
Turesson, Ingemar
Vangsted, Annette
Vogel, Ulla
Waage, Anders
Walker, Brian A
Wihlborg, Anna-Karin
Broyl, Annemiek
Davies, Faith E
Thorsteinsdottir, Unnur
Langer, Christian
Hansson, Markus
Kaiser, Martin
Sonneveld, Pieter
Stefansson, Kari
Morgan, Gareth J
Goldschmidt, Hartmut
Hemminki, Kari
Nilsson, Björn
Houlston, Richard S
Issue Date
2016
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Genome-wide association study identifies multiple susceptibility loci for multiple myeloma. 2016, 7:12050 Nat CommunAbstract
Multiple myeloma (MM) is a plasma cell malignancy with a significant heritable basis. Genome-wide association studies have transformed our understanding of MM predisposition, but individual studies have had limited power to discover risk loci. Here we perform a meta-analysis of these GWAS, add a new GWAS and perform replication analyses resulting in 9,866 cases and 239,188 controls. We confirm all nine known risk loci and discover eight new loci at 6p22.3 (rs34229995, P=1.31 × 10(-8)), 6q21 (rs9372120, P=9.09 × 10(-15)), 7q36.1 (rs7781265, P=9.71 × 10(-9)), 8q24.21 (rs1948915, P=4.20 × 10(-11)), 9p21.3 (rs2811710, P=1.72 × 10(-13)), 10p12.1 (rs2790457, P=1.77 × 10(-8)), 16q23.1 (rs7193541, P=5.00 × 10(-12)) and 20q13.13 (rs6066835, P=1.36 × 10(-13)), which localize in or near to JARID2, ATG5, SMARCD3, CCAT1, CDKN2A, WAC, RFWD3 and PREX1. These findings provide additional support for a polygenic model of MM and insight into the biological basis of tumour development.Description
To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.Additional Links
http://dx.doi.org/ 10.1038/ncomms12050https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932178/
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Archived with thanks to Nature communicationsae974a485f413a2113503eed53cd6c53
10.1038/ncomms12050
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