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@ARTICLE{Weigel:130847,
      author       = {C. Weigel$^*$ and M. R. Veldwijk and C. C. Oakes$^*$ and P.
                      Seibold$^*$ and A. Slynko$^*$ and D. B. Liesenfeld$^*$ and
                      M. Rabionet$^*$ and S. Hanke$^*$ and F. Wenz and E. Sperk
                      and A. Benner$^*$ and C. Rösli$^*$ and R. Sandhoff$^*$ and
                      Y. Assenov$^*$ and C. Plass$^*$ and C. Herskind and J.
                      Chang-Claude$^*$ and P. Schmezer$^*$ and O. Popanda$^*$},
      title        = {{E}pigenetic regulation of diacylglycerol kinase alpha
                      promotes radiation-induced fibrosis.},
      journal      = {Nature Communications},
      volume       = {7},
      number       = {NN},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-05925},
      pages        = {10893 -},
      year         = {2016},
      abstract     = {Radiotherapy is a fundamental part of cancer treatment but
                      its use is limited by the onset of late adverse effects in
                      the normal tissue, especially radiation-induced fibrosis.
                      Since the molecular causes for fibrosis are largely unknown,
                      we analyse if epigenetic regulation might explain
                      inter-individual differences in fibrosis risk. DNA
                      methylation profiling of dermal fibroblasts obtained from
                      breast cancer patients prior to irradiation identifies
                      differences associated with fibrosis. One region is
                      characterized as a differentially methylated enhancer of
                      diacylglycerol kinase alpha (DGKA). Decreased DNA
                      methylation at this enhancer enables recruitment of the
                      profibrotic transcription factor early growth response 1
                      (EGR1) and facilitates radiation-induced DGKA transcription
                      in cells from patients later developing fibrosis.
                      Conversely, inhibition of DGKA has pronounced effects on
                      diacylglycerol-mediated lipid homeostasis and reduces
                      profibrotic fibroblast activation. Collectively, DGKA is an
                      epigenetically deregulated kinase involved in radiation
                      response and may serve as a marker and therapeutic target
                      for personalized radiotherapy.},
      keywords     = {EGR1 protein, human (NLM Chemicals) / Early Growth Response
                      Protein 1 (NLM Chemicals) / RNA, Messenger (NLM Chemicals) /
                      Diacylglycerol Kinase (NLM Chemicals)},
      cin          = {C010 / C020 / C060 / G110 / G131 / A010 / V960},
      ddc          = {500},
      cid          = {I:(DE-He78)C010-20160331 / I:(DE-He78)C020-20160331 /
                      I:(DE-He78)C060-20160331 / I:(DE-He78)G110-20160331 /
                      I:(DE-He78)G131-20160331 / I:(DE-He78)A010-20160331 /
                      I:(DE-He78)V960-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26964756},
      pmc          = {pmc:PMC4792958},
      doi          = {10.1038/ncomms10893},
      url          = {https://inrepo02.dkfz.de/record/130847},
}