Genetic overlap between autoimmune diseases and non‐Hodgkin lymphoma subtypes

Lennox Din Mohammad Sheikh Nikitha Kosaraju Karin Ekström Smedby 1 Sasha Bernatsky 2 Sonja Berndt 3 Christine Skibola 4 Alexandra Nieters 5 Sophia Wang James Mckay 6 Pierluigi Cocco 7 Marc Maynadié 8 Lenka Foretova 9 Anthony Staines 10 Thomas Mack Silvia Sanjosé Timothy Vyse 11 Leonid Padyukov 12 Alain Monnereau 13 Alan Arslan Amy Moore 14 Angela Brooks‐wilson Anne Novak Bengt Glimelius 15 Brenda Birmann Brian Link 16 Carolyn Stewart Claire Vajdic Corinne Haioun 17 Corrado Magnani David Conti David Cox 18 Delphine Casabonne Demetrius Albanes 19 Eleanor Kane Eve Roman 20 Giacomo Muzi Gilles Salles 21 Graham Giles 22 Hans‐olov Adami Hervé Ghesquieres 23 Immaculata Vivo Jacqueline Clavel 13 James Cerhan 24 John Spinelli Jonathan Hofmann 25 Joseph Vijai 26 Karen Curtin 27 Karen Costenbader Kenan Onel Kenneth Offit 28 Lauren Teras Lindsay Morton 3 Lucia Conde Lucia Miligi 29 Mads Melbye 30 Maria Grazia Ennas 31 Mark Liebow Mark Purdue 3 Martha Glenn 27 Melissa Southey 32 Morris Din Nathaniel Rothman 3 Nicola Camp Nicole Wong Doo Nikolaus Becker 33 Nisha Pradhan Paige Bracci Paolo Boffetta 34 Paolo Vineis 35 Paul Brennan 6 Peter Kraft 36 Qing Lan Richard Severson 37 Roel Vermeulen 38 Roger Milne 39 Rudolph Kaaks Ruth Travis 40 Stephanie Weinstein Stephen Chanock 41 Stephen Ansell 24 Susan Slager 24 Tongzhang Zheng Yawei Zhang 42 Yolanda Benavente 43 Zachary Taub Lohith Madireddy Pierre‐antoine Gourraud Jorge Oksenberg 44 Wendy Cozen 45 Henrik Hjalgrim Pouya Khankhanian 44
Abstract : Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p = .0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.
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https://www.hal.inserm.fr/inserm-02286174
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Submitted on : Friday, September 13, 2019 - 2:44:45 PM
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Lennox Din, Mohammad Sheikh, Nikitha Kosaraju, Karin Ekström Smedby, Sasha Bernatsky, et al.. Genetic overlap between autoimmune diseases and non‐Hodgkin lymphoma subtypes. Genetic Epidemiology, Wiley, 2019, ⟨10.1002/gepi.22242⟩. ⟨inserm-02286174⟩

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