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@ARTICLE{Moore:176989,
      author       = {A. Moore and M. J. Machiela and M. Machado and S. S. Wang
                      and E. Kane and S. L. Slager and W. Zhou and M. Carrington
                      and Q. Lan and R. L. Milne and B. M. Birmann and H.-O. Adami
                      and D. Albanes and A. A. Arslan and N. Becker$^*$ and Y.
                      Benavente and S. Bisanzi and P. Boffetta and P. M. Bracci
                      and P. Brennan and A. R. Brooks-Wilson and F. Canzian$^*$
                      and N. Caporaso and J. Clavel and P. Cocco and L. Conde and
                      D. G. Cox and W. Cozen and K. Curtin and I. De Vivo and S.
                      de Sanjose and L. Foretova and S. M. Gapstur and H.
                      Ghesquières and G. G. Giles and M. Glenn and B. Glimelius
                      and C. Gao and T. M. Habermann and H. Hjalgrim and R. D.
                      Jackson and M. Liebow and B. K. Link and M. Maynadie and J.
                      McKay and M. Melbye and L. Miligi and T. J. Molina and A.
                      Monnereau and A. Nieters and K. E. North and K. Offit and A.
                      V. Patel and S. Piro and V. Ravichandran and E. Riboli and
                      G. Salles and R. K. Severson and C. F. Skibola and K. E.
                      Smedby and M. C. Southey and J. J. Spinelli and A. Staines
                      and C. Stewart and L. R. Teras and L. F. Tinker and R. C.
                      Travis and C. M. Vajdic and R. C. H. Vermeulen and J. Vijai
                      and E. Weiderpass and S. Weinstein and N. W. Doo and Y.
                      Zhang and T. Zheng and S. J. Chanock and N. Rothman and J.
                      R. Cerhan and M. Dean and N. J. Camp and M. Yeager and S. I.
                      Berndt},
      title        = {{G}enome-wide homozygosity and risk of four non-{H}odgkin
                      lymphoma subtypes.},
      journal      = {Journal of Translational Genetics and Genomics},
      volume       = {5},
      issn         = {2578-5281},
      address      = {Erscheinungsort nicht ermittelbar},
      reportid     = {DKFZ-2021-02222},
      pages        = {200-217},
      year         = {2021},
      note         = {Journal of Translational Genetics and Genomics (jtgg) =
                      2578-5281 (import from CrossRef, PubMed, , Journals:
                      inrepo01.inet.dkfz-heidelberg.de)},
      abstract     = {Recessive genetic variation is thought to play a role in
                      non-Hodgkin lymphoma (NHL) etiology. Runs of homozygosity
                      (ROH), defined based on long, continuous segments of
                      homozygous SNPs, can be used to estimate both measured and
                      unmeasured recessive genetic variation. We sought to examine
                      genome-wide homozygosity and NHL risk.We used data from
                      eight genome-wide association studies of four common NHL
                      subtypes: 3061 chronic lymphocytic leukemia (CLL), 3814
                      diffuse large B-cell lymphoma (DLBCL), 2784 follicular
                      lymphoma (FL), and 808 marginal zone lymphoma (MZL) cases,
                      as well as 9374 controls. We examined the effect of
                      homozygous variation on risk by: (1) estimating the fraction
                      of the autosome containing runs of homozygosity (FROH); (2)
                      calculating an inbreeding coefficient derived from the
                      correlation among uniting gametes (F3); and (3) examining
                      specific autosomal regions containing ROH. For each, we
                      calculated beta coefficients and standard errors using
                      logistic regression and combined estimates across studies
                      using random-effects meta-analysis.We discovered positive
                      associations between FROH and CLL (β = 21.1, SE = 4.41, P =
                      1.6 × 10-6) and FL (β = 11.4, SE = 5.82, P = 0.02) but not
                      DLBCL (P = 1.0) or MZL (P = 0.91). For F3, we observed an
                      association with CLL (β = 27.5, SE = 6.51, P = 2.4 ×
                      10-5). We did not find evidence of associations with
                      specific ROH, suggesting that the associations observed with
                      FROH and F3 for CLL and FL risk were not driven by a single
                      region of homozygosity.Our findings support the role of
                      recessive genetic variation in the etiology of CLL and FL;
                      additional research is needed to identify the specific loci
                      associated with NHL risk.},
      keywords     = {Non-Hodgkin lymphoma (Other) / chronic lymphocytic leukemia
                      (Other) / diffuse large B-cell lymphoma (Other) / follicular
                      lymphoma (Other) / homozygosity (Other) / marginal zone
                      lymphoma (Other)},
      cin          = {C020 / C055},
      cid          = {I:(DE-He78)C020-20160331 / I:(DE-He78)C055-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34622145},
      pmc          = {pmc:PMC8494431},
      doi          = {10.20517/jtgg.2021.08},
      url          = {https://inrepo02.dkfz.de/record/176989},
}