Genome-wide association study of classical Hodgkin lymphoma identifies key regulators of disease susceptibility.

Authors:
Amit Sud
Amit Sud
University of Manchester
United Kingdom
Hauke Thomsen, Dr.
Hauke Thomsen, Dr.
GeneWerk GmbH
Senior Bioinformatician
Bioinformatics, Biostatistics, Genetics
Heidelberg, Baden-Württemberg/Germany | Germany
Philip J Law
Philip J Law
The Institute of Cancer Research
Sutton | United Kingdom
Amy Holroyd
Amy Holroyd
Institute of Cancer Research
United Kingdom
Peter Broderick
Peter Broderick
Institute of Cancer Research
United Kingdom
Giulia Orlando
Giulia Orlando
Gray Institute for Radiation Oncology and Biology

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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Source
http://dx.doi.org/10.1038/s41467-017-00320-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5711884PMC

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December 2017
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