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@ARTICLE{Wu:157425,
      author       = {L. Wu and Y. Yang and X. Guo and X.-O. Shu and Q. Cai and
                      X. Shu and B. Li and R. Tao and C. Wu and J. B. Nikas and Y.
                      Sun and J. Zhu and M. J. Roobol and G. G. Giles and H.
                      Brenner$^*$ and E. M. John and J. Clements and E. M.
                      Grindedal and J. Y. Park and J. L. Stanford and Z.
                      Kote-Jarai and C. A. Haiman and R. A. Eeles and W. Zheng and
                      J. Long and R. A. Eeles and B. E. Henderson and C. A. Haiman
                      and Z. Kote-Jarai and F. R. Schumacher and D. Easton and S.
                      Benlloch and A. A. A. Olama and K. Muir and S. I. Berndt and
                      D. V. Conti and F. Wiklund and S. Chanock and S. M. Gapstur
                      and V. L. Stevens and C. M. Tangen and J. Batra and J.
                      Clements and H. Gronberg and N. Pashayan 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. S. 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 M.
                      Gamulin 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 and D. J. Hunter and W. J. Blot and E.
                      Riboli and R. A. Eeles and Z. Kote-Jarai and C. West and D.
                      E. Neal and F. C. Hamdy and J. L. Donovan and R. C. Travis
                      and E. Riboli and B. E. Henderson and C. A. Haiman and F. R.
                      Schumacher and S. I. Berndt and S. Chanock and S. M. Gapstur
                      and V. L. Stevens and D. Albanes and S. Weinstein and L.
                      Mucci and S. Koutros and R. C. Travis and K. L. Penney and
                      D. J. Hunter and E. Riboli and F. Wiklund and H. Gronberg
                      and S. I. Berndt and S. Chanock and D. Albanes and S.
                      Weinstein and S. Koutros},
      collaboration = {P. consortium and C. Consortium and B. Consortium and C.
                      Consortium and P. Consortium},
      title        = {{A}n integrative multi-omics analysis to identify candidate
                      {DNA} methylation biomarkers related to prostate cancer
                      risk.},
      journal      = {Nature Communications},
      volume       = {11},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2020-01620},
      pages        = {3905},
      year         = {2020},
      abstract     = {It remains elusive whether some of the associations
                      identified in genome-wide association studies of prostate
                      cancer (PrCa) may be due to regulatory effects of genetic
                      variants on CpG sites, which may further influence
                      expression of PrCa target genes. To search for CpG sites
                      associated with PrCa risk, here we establish genetic models
                      to predict methylation (N = 1,595) and conduct
                      association analyses with PrCa risk (79,194 cases and 61,112
                      controls). We identify 759 CpG sites showing an association,
                      including 15 located at novel loci. Among those 759 CpG
                      sites, methylation of 42 is associated with expression of 28
                      adjacent genes. Among 22 genes, 18 show an association with
                      PrCa risk. Overall, 25 CpG sites show consistent association
                      directions for the methylation-gene expression-PrCa pathway.
                      We identify DNA methylation biomarkers associated with PrCa,
                      and our findings suggest that specific CpG sites may
                      influence PrCa via regulating expression of candidate PrCa
                      target genes.},
      cin          = {C070 / C120 / HD01},
      ddc          = {500},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)HD01-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32764609},
      doi          = {10.1038/s41467-020-17673-9},
      url          = {https://inrepo02.dkfz.de/record/157425},
}