Genome-wide association study of classical Hodgkin lymphoma identifies key regulators of disease susceptibility.
Authors:
Oleg Lenive Lauren Wright Rosie Cooke Douglas Easton Paul Pharoah Alison Dunning Julian Peto Federico Canzian Rosalind Eeles ZSofia Kote-Jarai Kenneth Muir Nora Pashayan Per Hoffmann Markus M Nöthen Karl-Heinz Jöckel Elke Pogge von Strandmann Tracy Lightfoot Eleanor Kane Eve Roman Annette Lake Dorothy Montgomery Ruth F Jarrett Anthony J Swerdlow Andreas Engert Nick Orr Kari Hemminki Richard S Houlston
Nat Commun 2017 12 1;8(1):1892. Epub 2017 Dec 1.
Division of Genetics and Epidemiology, The Institute of Cancer Research, London, SW7 3RP, UK.
Several susceptibility loci for classical Hodgkin lymphoma have been reported. However, much of the heritable risk is unknown. Here, we perform a meta-analysis of two existing genome-wide association studies, a new genome-wide association study, and replication totalling 5,314 cases and 16,749 controls. We identify risk loci for all classical Hodgkin lymphoma at 6q22.33 (rs9482849, P = 1.52 × 10) and for nodular sclerosis Hodgkin lymphoma at 3q28 (rs4459895, P = 9.43 × 10), 6q23.3 (rs6928977, P = 4.62 × 10), 10p14 (rs3781093, P = 9.49 × 10), 13q34 (rs112998813, P = 4.58 × 10) and 16p13.13 (rs34972832, P = 2.12 × 10). Additionally, independent loci within the HLA region are observed for nodular sclerosis Hodgkin lymphoma (rs9269081, HLA-DPB1*03:01, Val86 in HLA-DRB1) and mixed cellularity Hodgkin lymphoma (rs1633096, rs13196329, Val86 in HLA-DRB1). The new and established risk loci localise to areas of active chromatin and show an over-representation of transcription factor binding for determinants of B-cell development and immune response.
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| http://dx.doi.org/10.1038/s41467-017-00320-1 | DOI Listing |
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5711884 | PMC |
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(Supplied by CrossRef)Article in Nature
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Nature 2010
The 1000 Genomes Project Consortium. A map of human genome variation from population-scale sequencing et al.
Nature 2010
