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@ARTICLE{Saunders:169730,
      author       = {C. N. Saunders and S. Chattopadhyay and S. Huhn and N.
                      Weinhold and P. Hoffmann and M. M. Nöthen and K.-H. Jöckel
                      and B. Schmidt and S. Landi and H. Goldschmidt and P. Milani
                      and G. Merlini and D. Rowcieno and P. Hawkins and U.
                      Hegenbart and G. Palladini and A. Wechalekar and S. O.
                      Schönland and A. Försti$^*$ and R. Houlston and K.
                      Hemminki$^*$},
      title        = {{S}earch for {AL} amyloidosis risk factors using
                      {M}endelian randomization.},
      journal      = {Blood advances},
      volume       = {5},
      number       = {13},
      issn         = {2473-9537},
      address      = {Washington, DC},
      publisher    = {American Society of Hematology},
      reportid     = {DKFZ-2021-01535},
      pages        = {2725 - 2731},
      year         = {2021},
      note         = {2021 Jul 13;5(13):2725-2731},
      abstract     = {In amyloid light chain (AL) amyloidosis, amyloid fibrils
                      derived from immunoglobulin light chain are deposited in
                      many organs, interfering with their function. The etiology
                      of AL amyloidosis is poorly understood. Summary data from
                      genome-wide association studies (GWASs) of multiple
                      phenotypes can be exploited by Mendelian randomization (MR)
                      methodology to search for factors influencing AL amyloidosis
                      risk. We performed a 2-sample MR analyzing 72 phenotypes,
                      proxied by 3461 genetic variants, and summary genetic data
                      from a GWAS of 1129 AL amyloidosis cases and 7589 controls.
                      Associations with a Bonferroni-defined significance level
                      were observed for genetically predicted increased monocyte
                      counts (P = 3.8 × 10-4) and the tumor necrosis factor
                      receptor superfamily member 17 (TNFRSF17) gene (P = 3.4 ×
                      10-5). Two other associations with the TNFRSF (members 6 and
                      19L) reached a nominal significance level. The association
                      between genetically predicted decreased fibrinogen levels
                      may be related to roles of fibrinogen other than blood
                      clotting. be related to its nonhemostatic role. It is
                      plausible that a causal relationship with monocyte
                      concentration could be explained by selection of a light
                      chain-producing clone during progression of monoclonal
                      gammopathy of unknown significance toward AL amyloidosis.
                      Because TNFRSF proteins have key functions in lymphocyte
                      biology, it is entirely plausible that they offer a
                      potential link to AL amyloidosis pathophysiology. Our study
                      provides insight into AL amyloidosis etiology, suggesting
                      high circulating levels of monocytes and TNFRSF proteins as
                      risk factors.},
      cin          = {B062 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34228109},
      doi          = {10.1182/bloodadvances.2021004423},
      url          = {https://inrepo02.dkfz.de/record/169730},
}