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

Clicks: 456
ID: 52689
2019
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #1 of 39 articles by views in genetic epidemiology

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
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.
Reference Key
din2019geneticgenetic Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors 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;de Sanjosé, Silvia;Vyse, Timothy J;Padyukov, Leonid;Monnereau, Alain;Arslan, Alan A;Moore, Amy;Brooks-Wilson, 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, Hans-Olov;Ghesquières, Hervé;De 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, Pierre-Antoine;Oksenberg, Jorge R;Cozen, Wendy;Hjalgrim, Henrik;Khankhanian, Pouya;
Journal genetic epidemiology
Year 2019
DOI
10.1002/gepi.22242
URL
Keywords

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.