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@ARTICLE{Rettig:127368,
      author       = {I. Rettig$^*$ and E. Koeneke$^*$ and F. Trippel$^*$ and W.
                      C. Mueller and J. Burhenne and A. Kopp-Schneider$^*$ and J.
                      Fabian$^*$ and A. Schober and U. Fernekorn and A. von
                      Deimling$^*$ and H. E. Deubzer$^*$ and T. Milde$^*$ and O.
                      Witt$^*$ and I. Oehme$^*$},
      title        = {{S}elective inhibition of {HDAC}8 decreases neuroblastoma
                      growth in vitro and in vivo and enhances retinoic
                      acid-mediated differentiation.},
      journal      = {Cell death $\&$ disease},
      volume       = {6},
      number       = {2},
      issn         = {2041-4889},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-03393},
      pages        = {e1657 -},
      year         = {2015},
      abstract     = {For differentiation-defective malignancies, compounds that
                      modulate transcription, such as retinoic acid and histone
                      deacetylase (HDAC) inhibitors, are of particular interest.
                      HDAC inhibitors are currently under investigation for the
                      treatment of a broad spectrum of cancer diseases. However,
                      one clinical drawback is class-specific toxicity of
                      unselective inhibitors, limiting their full anticancer
                      potential. Selective targeting of individual HDAC isozymes
                      in defined tumor entities may therefore be an attractive
                      alternative treatment approach. We have previously
                      identified HDAC family member 8 (HDAC8) as a novel target in
                      childhood neuroblastoma. Using small-molecule inhibitors, we
                      now demonstrate that selective inhibition of HDAC8 exhibits
                      antineuroblastoma activity without toxicity in two xenograft
                      mouse models of MYCN oncogene-amplified neuroblastoma. In
                      contrast, the unselective HDAC inhibitor vorinostat was more
                      toxic in the same models. HDAC8-selective inhibition induced
                      cell cycle arrest and differentiation in vitro and in vivo.
                      Upon combination with retinoic acid, differentiation was
                      significantly enhanced, as demonstrated by elongated
                      neurofilament-positive neurites and upregulation of NTRK1.
                      Additionally, MYCN oncogene expression was downregulated in
                      vitro and tumor cell growth was markedly reduced in vivo.
                      Mechanistic studies suggest that cAMP-response
                      element-binding protein (CREB) links HDAC8- and retinoic
                      acid-mediated gene transcription. In conclusion,
                      HDAC-selective targeting can be effective in tumors
                      exhibiting HDAC isozyme-dependent tumor growth in vivo and
                      can be combined with differentiation-inducing agents.},
      keywords     = {Histone Deacetylase Inhibitors (NLM Chemicals) / Hydroxamic
                      Acids (NLM Chemicals) / Indoles (NLM Chemicals) / PCI 34051
                      (NLM Chemicals) / Repressor Proteins (NLM Chemicals) /
                      Tretinoin (NLM Chemicals) / HDAC8 protein, human (NLM
                      Chemicals) / HDAC8 protein, mouse (NLM Chemicals) / Histone
                      Deacetylases (NLM Chemicals)},
      cin          = {G340 / C060 / G380},
      ddc          = {570},
      cid          = {I:(DE-He78)G340-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)G380-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25695609},
      pmc          = {pmc:PMC4669789},
      doi          = {10.1038/cddis.2015.24},
      url          = {https://inrepo02.dkfz.de/record/127368},
}