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@ARTICLE{Went:137635,
      author       = {M. Went and A. Sud and A. Försti$^*$ and B.-M. Halvarsson
                      and N. Weinhold and S. Kimber and M. van Duin and G.
                      Thorleifsson and A. Holroyd and D. C. Johnson and N. Li and
                      G. Orlando and P. J. Law and M. Ali and B. Chen$^*$ and J.
                      S. Mitchell and D. F. Gudbjartsson and R. Kuiper and O. W.
                      Stephens and U. Bertsch and P. Broderick and C. Campo$^*$
                      and O. R. Bandapalli and H. Einsele and W. A. Gregory and U.
                      Gullberg and J. Hillengass and P. Hoffmann and G. H. Jackson
                      and K.-H. Jöckel and E. Johnsson and S. Y. Kristinsson and
                      U.-H. Mellqvist and H. Nahi and D. Easton and P. Pharoah and
                      A. Dunning and J. Peto and F. Canzian$^*$ and A. Swerdlow
                      and R. A. Eeles and Z. Kote-Jarai and K. Muir and N.
                      Pashayan and J. Nickel and M. M. Nöthen and T. Rafnar and
                      F. M. Ross and M. I. da Silva Filho$^*$ and H. Thomsen$^*$
                      and I. Turesson and A. Vangsted and N. F. Andersen and A.
                      Waage and B. A. Walker and A.-K. Wihlborg and A. Broyl and
                      F. E. Davies and U. Thorsteinsdottir and C. Langer and M.
                      Hansson and H. Goldschmidt$^*$ and M. Kaiser and P.
                      Sonneveld and K. Stefansson and G. J. Morgan and K.
                      Hemminki$^*$ and B. Nilsson and R. S. Houlston and B. E.
                      Henderson and C. A. Haiman and S. Benlloch and F. R.
                      Schumacher and A. A. A. Olama and S. I. Berndt and D. V.
                      Conti and F. Wiklund and S. Chanock and V. L. Stevens and C.
                      M. Tangen and J. Batra and J. Clements and H. Gronberg and
                      J. Schleutker and D. Albanes and S. Weinstein and A. Wolk
                      and C. West and L. Mucci and G. Cancel-Tassin and S. Koutros
                      and K. D. Sorensen and E. M. Grindedal and D. E. Neal and F.
                      C. Hamdy and J. L. Donovan and R. C. Travis and R. J.
                      Hamilton and S. A. Ingles and B. Rosenstein and Y.-J. Lu and
                      G. G. Giles and A. S. Kibel and A. Vega and M. Kogevinas and
                      K. L. Penney and J. Y. Park and J. L. Stanford and C.
                      Cybulski and B. G. Nordestgaard and H. Brenner$^*$ and C.
                      Maier and J. Kim and E. M. John and M. R. Teixeira and S. L.
                      Neuhausen and K. De Ruyck and A. Razack and L. F. Newcomb
                      and D. Lessel and R. Kaneva and N. Usmani and F. Claessens
                      and P. A. Townsend and M. G. Dominguez and M. J. Roobol and
                      F. Menegaux and K.-T. Khaw and L. Cannon-Albright and H.
                      Pandha and S. N. Thibodeau},
      collaboration = {P. consortium},
      title        = {{I}dentification of multiple risk loci and regulatory
                      mechanisms influencing susceptibility to multiple myeloma.},
      journal      = {Nature Communications},
      volume       = {9},
      number       = {1},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2018-01515},
      pages        = {3707},
      year         = {2018},
      abstract     = {Genome-wide association studies (GWAS) have transformed our
                      understanding of susceptibility to multiple myeloma (MM),
                      but much of the heritability remains unexplained. We report
                      a new GWAS, a meta-analysis with previous GWAS and a
                      replication series, totalling 9974 MM cases and 247,556
                      controls of European ancestry. Collectively, these data
                      provide evidence for six new MM risk loci, bringing the
                      total number to 23. Integration of information from gene
                      expression, epigenetic profiling and in situ Hi-C data for
                      the 23 risk loci implicate disruption of developmental
                      transcriptional regulators as a basis of MM susceptibility,
                      compatible with altered B-cell differentiation as a key
                      mechanism. Dysregulation of autophagy/apoptosis and cell
                      cycle signalling feature as recurrently perturbed pathways.
                      Our findings provide further insight into the biological
                      basis of MM.},
      cin          = {C055 / C050 / C070},
      ddc          = {500},
      cid          = {I:(DE-He78)C055-20160331 / I:(DE-He78)C050-20160331 /
                      I:(DE-He78)C070-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30213928},
      pmc          = {pmc:PMC6137048},
      doi          = {10.1038/s41467-018-04989-w},
      url          = {https://inrepo02.dkfz.de/record/137635},
}