Literature DB >> 31407831

Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes.

Lennox Din1, Mohammad Sheikh1, Nikitha Kosaraju2, Karin Ekstrom Smedby3, Sasha Bernatsky4,5, Sonja I Berndt6, Christine F Skibola7, Alexandra Nieters8, Sophia Wang9, James D McKay10, Pierluigi Cocco11, Marc Maynadié12, Lenka Foretová13, Anthony Staines14, Thomas M Mack15, Silvia de Sanjosé16,17,18, Timothy J Vyse19, Leonid Padyukov20, Alain Monnereau21,22, Alan A Arslan23, Amy Moore6, Angela R Brooks-Wilson24,25, Anne J Novak26, Bengt Glimelius27, Brenda M Birmann28, Brian K Link29, Carolyn Stewart30, Claire M Vajdic31, Corinne Haioun32, Corrado Magnani33, David V Conti34, David G Cox35, Delphine Casabonne17,18, Demetrius Albanes6, Eleanor Kane36, Eve Roman36, Giacomo Muzi37, Gilles Salles38, Graham G Giles39,40, Hans-Olov Adami41,42, Hervé Ghesquières38, Immaculata De Vivo28,43, Jacqueline Clavel44, James R Cerhan45, John J Spinelli46,47, Jonathan Hofmann6, Joseph Vijai30, Karen Curtin48, Karen H Costenbader28, Kenan Onel49, Kenneth Offit50,51, Lauren R Teras52, Lindsay Morton6, Lucia Conde53, Lucia Miligi54, Mads Melbye55,56, Maria Grazia Ennas57, Mark Liebow26, Mark P Purdue58, Martha Glenn48, Melissa C Southey59,60, Morris Din61, Nathaniel Rothman6, Nicola J Camp48,62, Nicole Wong Doo63,64, Nikolaus Becker65, Nisha Pradhan30, Paige M Bracci66, Paolo Boffetta67, Paolo Vineis68, Paul Brennan10, Peter Kraft69, Qing Lan6, Richard K Severson70, Roel C H Vermeulen71, Roger L Milne39,40,64, Rudolph Kaaks72, Ruth C Travis73, Stephanie J Weinstein6, Stephen J Chanock6, Stephen M Ansell26, Susan L Slager45, Tongzhang Zheng74, Yawei Zhang75, Yolanda Benavente17,18, Zachary Taub76, Lohith Madireddy77, Pierre-Antoine Gourraud78,79, Jorge R Oksenberg77, Wendy Cozen80, Henrik Hjalgrim55, Pouya Khankhanian2.   

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.
© 2019 Wiley Periodicals, Inc.

Entities:  

Keywords:  autoimmune disease; genome-wide association study; meta-analysis; non-Hodgkin lymphoma

Mesh：

Substances：

Year:  2019        PMID： 31407831      PMCID： PMC6763347          DOI： 10.1002/gepi.22242

Source DB:  PubMed          Journal:  Genet Epidemiol        ISSN： 0741-0395            Impact factor:   2.344


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