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@ARTICLE{Ajore:178451,
      author       = {R. Ajore and A. Niroula and M. Pertesi and C. Cafaro and M.
                      Thodberg and M. Went and E. L. Bao and L. Duran-Lozano and
                      A. Lopez de Lapuente Portilla and T. Olafsdottir and N.
                      Ugidos-Damboriena and O. Magnusson and M. Samur and C. A.
                      Lareau and G. H. Halldorsson and G. Thorleifsson and G. L.
                      Norddahl and K. Gunnarsdottir and A. Försti$^*$ and H.
                      Goldschmidt and K. Hemminki$^*$ and F. van Rhee and S.
                      Kimber and A. S. Sperling and M. Kaiser and K. Anderson and
                      I. Jonsdottir and N. Munshi and T. Rafnar and A. Waage and
                      N. Weinhold$^*$ and U. Thorsteinsdottir and V. G. Sankaran
                      and K. Stefansson and R. Houlston and B. Nilsson},
      title        = {{F}unctional dissection of inherited non-coding variation
                      influencing multiple myeloma risk.},
      journal      = {Nature Communications},
      volume       = {13},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2022-00077},
      pages        = {151},
      year         = {2022},
      abstract     = {Thousands of non-coding variants have been associated with
                      increased risk of human diseases, yet the causal variants
                      and their mechanisms-of-action remain obscure. In an
                      integrative study combining massively parallel reporter
                      assays (MPRA), expression analyses (eQTL, meQTL, PCHiC) and
                      chromatin accessibility analyses in primary cells (caQTL),
                      we investigate 1,039 variants associated with multiple
                      myeloma (MM). We demonstrate that MM susceptibility is
                      mediated by gene-regulatory changes in plasma cells and
                      B-cells, and identify putative causal variants at six risk
                      loci (SMARCD3, WAC, ELL2, CDCA7L, CEP120, and PREX1).
                      Notably, three of these variants co-localize with
                      significant plasma cell caQTLs, signaling the presence of
                      causal activity at these precise genomic positions in an
                      endogenous chromosomal context in vivo. Our results provide
                      a systematic functional dissection of risk loci for a
                      hematologic malignancy.},
      cin          = {B062 / C020},
      ddc          = {500},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)C020-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35013207},
      doi          = {10.1038/s41467-021-27666-x},
      url          = {https://inrepo02.dkfz.de/record/178451},
}