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@ARTICLE{Brocks:124453,
      author       = {D. Brocks$^*$ and C. R. Schmidt$^*$ and M. Daskalakis$^*$
                      and H. S. Jang and N. M. Shah and D. Li and J. Li and B.
                      Zhang and Y. Hou and S. Laudato$^*$ and D. Lipka$^*$ and J.
                      Schott$^*$ and H. Bierhoff$^*$ and Y. Assenov$^*$ and M.
                      Helf$^*$ and A. Ressnerova$^*$ and M. S. Islam$^*$ and A. M.
                      Lindroth$^*$ and S. Haas$^*$ and M. Essers$^*$ and C. D.
                      Imbusch$^*$ and B. Brors$^*$ and I. Oehme$^*$ and O.
                      Witt$^*$ and M. Lübbert$^*$ and J.-P. Mallm$^*$ and K.
                      Rippe$^*$ and R. Will$^*$ and D. Weichenhan$^*$ and G.
                      Stoecklin and C. Gerhäuser$^*$ and C. C. Oakes$^*$ and T.
                      Wang and C. Plass$^*$},
      title        = {{DNMT} and {HDAC} inhibitors induce cryptic transcription
                      start sites encoded in long terminal repeats.},
      journal      = {Nature genetics},
      volume       = {49},
      number       = {7},
      issn         = {1546-1718},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DKFZ-2017-01330},
      pages        = {1052 - 1060},
      year         = {2017},
      abstract     = {Several mechanisms of action have been proposed for DNA
                      methyltransferase and histone deacetylase inhibitors (DNMTi
                      and HDACi), primarily based on candidate-gene approaches.
                      However, less is known about their genome-wide
                      transcriptional and epigenomic consequences. By mapping
                      global transcription start site (TSS) and chromatin
                      dynamics, we observed the cryptic transcription of thousands
                      of treatment-induced non-annotated TSSs (TINATs) following
                      DNMTi and HDACi treatment. The resulting transcripts
                      frequently splice into protein-coding exons and encode
                      truncated or chimeric ORFs translated into products with
                      predicted abnormal or immunogenic functions. TINAT
                      transcription after DNMTi treatment coincided with DNA
                      hypomethylation and gain of classical promoter histone
                      marks, while HDACi specifically induced a subset of TINATs
                      in association with H2AK9ac, H3K14ac, and H3K23ac. Despite
                      this mechanistic difference, both inhibitors convergently
                      induced transcription from identical sites, as we found
                      TINATs to be encoded in solitary long terminal repeats of
                      the ERV9/LTR12 family, which are epigenetically repressed in
                      virtually all normal cells.},
      cin          = {C010 / V960 / G200 / G340 / B066 / A200 / A030 / L101 /
                      L601},
      ddc          = {570},
      cid          = {I:(DE-He78)C010-20160331 / I:(DE-He78)V960-20160331 /
                      I:(DE-He78)G200-20160331 / I:(DE-He78)G340-20160331 /
                      I:(DE-He78)B066-20160331 / I:(DE-He78)A200-20160331 /
                      I:(DE-He78)A030-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)L601-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28604729},
      doi          = {10.1038/ng.3889},
      url          = {https://inrepo02.dkfz.de/record/124453},
}