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Genetic overlap between autoimmune diseases and non‐Hodgkin lymphoma subtypes
Author(s) -
Din Lennox,
Sheikh Mohammad,
Kosaraju Nikitha,
Smedby Karin Ekstrom,
Bernatsky Sasha,
Berndt Sonja I.,
Skibola Christine F.,
Nieters Alexandra,
Wang Sophia,
McKay James D.,
Cocco Pierluigi,
Maynadié Marc,
Foretová Lenka,
Staines Anthony,
Mack Thomas M.,
Sanjosé Silvia,
Vyse Timothy J.,
Padyukov Leonid,
Monnereau Alain,
Arslan Alan A.,
Moore Amy,
BrooksWilson Angela R.,
Novak Anne J.,
Glimelius Bengt,
Birmann Brenda M.,
Link Brian K.,
Stewart Carolyn,
Vajdic Claire M.,
Haioun Corinne,
Magnani Corrado,
Conti David V.,
Cox David G.,
Casabonne Delphine,
Albanes Demetrius,
Kane Eleanor,
Roman Eve,
Muzi Giacomo,
Salles Gilles,
Giles Graham G.,
Adami HansOlov,
Ghesquières Hervé,
Vivo Immaculata,
Clavel Jacqueline,
Cerhan James R.,
Spinelli John J.,
Hofmann Jonathan,
Vijai Joseph,
Curtin Karen,
Costenbader Karen H.,
Onel Kenan,
Offit Kenneth,
Teras Lauren R.,
Morton Lindsay,
Conde Lucia,
Miligi Lucia,
Melbye Mads,
Ennas Maria Grazia,
Liebow Mark,
Purdue Mark P.,
Glenn Martha,
Southey Melissa C.,
Din Morris,
Rothman Nathaniel,
Camp Nicola J.,
Wong Doo Nicole,
Becker Nikolaus,
Pradhan Nisha,
Bracci Paige M.,
Boffetta Paolo,
Vineis Paolo,
Brennan Paul,
Kraft Peter,
Lan Qing,
Severson Richard K.,
Vermeulen Roel C. H.,
Milne Roger L.,
Kaaks Rudolph,
Travis Ruth C.,
Weinstein Stephanie J.,
Chanock Stephen J.,
Ansell Stephen M.,
Slager Susan L.,
Zheng Tongzhang,
Zhang Yawei,
Benavente Yolanda,
Taub Zachary,
Madireddy Lohith,
Gourraud PierreAntoine,
Oksenberg Jorge R.,
Cozen Wendy,
Hjalgrim Henrik,
Khankhanian Pouya
Publication year - 2019
Publication title -
genetic epidemiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.301
H-Index - 98
eISSN - 1098-2272
pISSN - 0741-0395
DOI - 10.1002/gepi.22242
Subject(s) - genome wide association study , lymphoma , disease , etiology , follicular lymphoma , genetic association , rheumatoid arthritis , medicine , oncology , immunology , biology , genetics , single nucleotide polymorphism , gene , genotype
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.