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@ARTICLE{Din:144594,
      author       = {L. Din and M. Sheikh and N. Kosaraju and K. E. Smedby and
                      S. Bernatsky and S. I. Berndt and C. F. Skibola and A.
                      Nieters and S. Wang and J. D. McKay and P. Cocco and M.
                      Maynadié and L. Foretová and A. Staines and T. M. Mack and
                      S. de Sanjosé and T. J. Vyse and L. Padyukov and A.
                      Monnereau and A. A. Arslan and A. Moore and A. R.
                      Brooks-Wilson and A. J. Novak and B. Glimelius and B. M.
                      Birmann and B. K. Link and C. Stewart and C. M. Vajdic and
                      C. Haioun and C. Magnani and D. V. Conti and D. G. Cox and
                      D. Casabonne and D. Albanes and E. Kane and E. Roman and G.
                      Muzi and G. Salles and G. G. Giles and H.-O. Adami and H.
                      Ghesquières and I. De Vivo and J. Clavel and J. R. Cerhan
                      and J. J. Spinelli and J. Hofmann and J. Vijai and K. Curtin
                      and K. H. Costenbader and K. Onel and K. Offit and L. R.
                      Teras and L. Morton and L. Conde and L. Miligi and M. Melbye
                      and M. G. Ennas and M. Liebow and M. P. Purdue and M. Glenn
                      and M. C. Southey and M. Din and N. Rothman and N. J. Camp
                      and N. Wong Doo and N. Becker$^*$ and N. Pradhan and P. M.
                      Bracci and P. Boffetta and P. Vineis and P. Brennan and P.
                      Kraft and Q. Lan and R. K. Severson and R. C. H. Vermeulen
                      and R. L. Milne and R. Kaaks$^*$ and R. C. Travis and S. J.
                      Weinstein and S. J. Chanock and S. M. Ansell and S. L.
                      Slager and T. Zheng and Y. Zhang and Y. Benavente and Z.
                      Taub and L. Madireddy and P.-A. Gourraud and J. R. Oksenberg
                      and W. Cozen and H. Hjalgrim and P. Khankhanian},
      title        = {{G}enetic overlap between autoimmune diseases and
                      non-{H}odgkin lymphoma subtypes.},
      journal      = {Genetic epidemiology},
      volume       = {43},
      number       = {7},
      issn         = {1098-2272},
      address      = {New York, NY},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2019-02036},
      pages        = {844-863},
      year         = {2019},
      note         = {Genet Epidemiol. 2019 Oct;43(7):844-863},
      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.},
      cin          = {C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C020-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31407831},
      doi          = {10.1002/gepi.22242},
      url          = {https://inrepo02.dkfz.de/record/144594},
}