% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Brocks:119711,
      author       = {D. Brocks$^*$ and Y. Assenov$^*$ and S. Minner and O.
                      Bogatyrova$^*$ and R. Simon and C. Koop and C. Oakes$^*$ and
                      M. Zucknick$^*$ and D. Lipka$^*$ and J. Weischenfeldt and L.
                      Feuerbach$^*$ and R. Cowper-Sal Lari and M. Lupien and B.
                      Brors$^*$ and J. Korbel and T. Schlomm and A. Tanay and G.
                      Sauter and C. Gerhäuser$^*$ and C. Plass$^*$ and I. E. O.
                      P. C. Project},
      title        = {{I}ntratumor {DNA} methylation heterogeneity reflects
                      clonal evolution in aggressive prostate cancer.080},
      journal      = {Cell reports},
      volume       = {8},
      number       = {3},
      issn         = {2211-1247},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-00338},
      pages        = {798 - 806},
      year         = {2014},
      abstract     = {Despite much evidence on epigenetic abnormalities in
                      cancer, it is currently unclear to what extent epigenetic
                      alterations can be associated with tumors' clonal genetic
                      origins. Here, we show that the prostate intratumor
                      heterogeneity in DNA methylation and copy-number patterns
                      can be explained by a unified evolutionary process. By
                      assaying multiple topographically distinct tumor sites,
                      premalignant lesions, and lymph node metastases within five
                      cases of prostate cancer, we demonstrate that both DNA
                      methylation and copy-number heterogeneity consistently
                      reflect the life history of the tumors. Furthermore, we show
                      cases of genetic or epigenetic convergent evolution and
                      highlight the diversity in the evolutionary origins and
                      aberration spectrum between tumor and metastatic subclones.
                      Importantly, DNA methylation can complement genetic data by
                      serving as a proxy for activity at regulatory domains, as we
                      show through identification of high epigenetic heterogeneity
                      at androgen-receptor-bound enhancers. Epigenome variation
                      thereby expands on the current genome-centric view on tumor
                      heterogeneity.},
      cin          = {C010 / C060 / B080 / G200 / L101},
      ddc          = {570},
      cid          = {I:(DE-He78)C010-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)B080-20160331 / I:(DE-He78)G200-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25066126},
      doi          = {10.1016/j.celrep.2014.06.053},
      url          = {https://inrepo02.dkfz.de/record/119711},
}