Genome-wide association study identifies multiple susceptibility loci for multiple myeloma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-07-01

AUTHORS

Jonathan S. Mitchell, Ni Li, Niels Weinhold, Asta Försti, Mina Ali, Mark van Duin, Gudmar Thorleifsson, David C. Johnson, Bowang Chen, Britt-Marie Halvarsson, Daniel F. Gudbjartsson, Rowan Kuiper, Owen W. Stephens, Uta Bertsch, Peter Broderick, Chiara Campo, Hermann Einsele, Walter A. Gregory, Urban Gullberg, Marc Henrion, Jens Hillengass, Per Hoffmann, Graham H. Jackson, Ellinor Johnsson, Magnus Jöud, Sigurður Y. Kristinsson, Stig Lenhoff, Oleg Lenive, Ulf-Henrik Mellqvist, Gabriele Migliorini, Hareth Nahi, Sven Nelander, Jolanta Nickel, Markus M. Nöthen, Thorunn Rafnar, Fiona M. Ross, Miguel Inacio da Silva Filho, Bhairavi Swaminathan, Hauke Thomsen, Ingemar Turesson, Annette Vangsted, Ulla Vogel, Anders Waage, Brian A. Walker, Anna-Karin Wihlborg, Annemiek Broyl, Faith E. Davies, Unnur Thorsteinsdottir, Christian Langer, Markus Hansson, Martin Kaiser, Pieter Sonneveld, Kari Stefansson, Gareth J. Morgan, Hartmut Goldschmidt, Kari Hemminki, Björn Nilsson, Richard S. Houlston

ABSTRACT

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. More... »

PAGES

12050

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    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms12050

    DOI

    http://dx.doi.org/10.1038/ncomms12050

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1039128645

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27363682


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