Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

Lennox Din, Mohammad Sheikh, Nikitha Kosaraju, Karin Ekstrom Smedby, Sasha Bernatsky, Sonja I. Berndt, Christine F. Skibola, Alexandra Nieters, Sophia Wang, James D. McKay, Pierluigi Cocco, Marc Maynadié, Lenka Foretová, Anthony Staines, Thomas M. Mack, Silvia de Sanjosé, Timothy J. Vyse, Leonid Padyukov, Alain Monnereau, Alan A. ArslanAmy Moore, Angela R. Brooks-Wilson, Anne J. Novak, Bengt Glimelius, Brenda M. Birmann, Brian K. Link, Carolyn Stewart, Claire M. Vajdic, Corinne Haioun, Corrado Magnani, David V. Conti, David G. Cox, Delphine Casabonne, Demetrius Albanes, Eleanor Kane, Eve Roman, Giacomo Muzi, Gilles Salles, Graham G. Giles, Hans Olov Adami, Hervé Ghesquières, Immaculata De Vivo, Jacqueline Clavel, James R. Cerhan, John J. Spinelli, Jonathan Hofmann, Joseph Vijai, Karen Curtin, Karen H. Costenbader, Kenan Onel, Kenneth Offit, Lauren R. Teras, Lindsay Morton, Lucia Conde, Lucia Miligi, Mads Melbye, Maria Grazia Ennas, Mark Liebow, Mark P. Purdue, Martha Glenn, Melissa C. Southey, Morris Din, Nathaniel Rothman, Nicola J. Camp, Nicole Wong Doo, Nikolaus Becker, Nisha Pradhan, Paige M. Bracci, Paolo Boffetta, Paolo Vineis, Paul Brennan, Peter Kraft, Qing Lan, Richard K. Severson, Roel C.H. Vermeulen, Roger L. Milne, Rudolph Kaaks, Ruth C. Travis, Stephanie J. Weinstein, Stephen J. Chanock, Stephen M. Ansell, Susan L. Slager, Tongzhang Zheng, Yawei Zhang, Yolanda Benavente, Zachary Taub, Lohith Madireddy, Pierre Antoine Gourraud, Jorge R. Oksenberg, Wendy Cozen, Henrik Hjalgrim, Pouya Khankhanian

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)844-863
Number of pages20
JournalGenetic epidemiology
Issue number7
StatePublished - Oct 1 2019


  • autoimmune disease
  • genome-wide association study
  • meta-analysis
  • non-Hodgkin lymphoma

ASJC Scopus subject areas

  • Epidemiology
  • Genetics(clinical)


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