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@ARTICLE{Dreidax:119889,
      author       = {D. Dreidax$^*$ and S. Bannert$^*$ and K.-O. Henrich$^*$ and
                      C. Schröder$^*$ and S. Bender$^*$ and C. C. Oakes$^*$ and
                      S. Lindner and J. H. Schulte and D. Duffy and T. Schwarzl
                      and M. Saadati$^*$ and V. Ehemann and A. Benner$^*$ and S.
                      Pfister$^*$ and M. Fischer and F. Westermann$^*$},
      title        = {p19-{INK}4d inhibits neuroblastoma cell growth, induces
                      differentiation and is hypermethylated and downregulated in
                      {MYCN}-amplified neuroblastomas.},
      journal      = {Human molecular genetics},
      volume       = {23},
      number       = {25},
      issn         = {1460-2083},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2017-00480},
      pages        = {6826 - 6837},
      year         = {2014},
      abstract     = {Uncontrolled cell cycle entry, resulting from deregulated
                      CDK-RB1-E2F pathway activity, is a crucial determinant of
                      neuroblastoma cell malignancy. Here we identify
                      neuroblastoma-suppressive functions of the p19-INK4d CDK
                      inhibitor and uncover mechanisms of its repression in
                      high-risk neuroblastomas. Reduced p19-INK4d expression was
                      associated with poor event-free and overall survival and
                      neuroblastoma risk factors including amplified MYCN in a set
                      of 478 primary neuroblastomas. High MYCN expression
                      repressed p19-INK4d mRNA and protein levels in different
                      neuroblastoma cell models with conditional MYCN expression.
                      MassARRAY and 450K methylation analyses of 105 primary
                      neuroblastomas uncovered a differentially methylated region
                      within p19-INK4d. Hypermethylation of this region was
                      associated with reduced p19-INK4d expression. In accordance,
                      p19-INK4d expression was activated upon treatment with the
                      demethylating agent, 2'-deoxy-5-azacytidine, in
                      neuroblastoma cell lines. Ectopic p19-INK4d expression
                      decreased viability, clonogenicity and the capacity for
                      anchorage-independent growth of neuroblastoma cells, and
                      shifted the cell cycle towards the G1/0 phase. p19-INK4d
                      also induced neurite-like processes and markers of neuronal
                      differentiation. Moreover, neuroblastoma cell
                      differentiation, induced by all-trans retinoic acid or
                      NGF-NTRK1-signaling, activated p19-INK4d expression. Our
                      findings pinpoint p19-INK4d as a neuroblastoma suppressor
                      and provide evidence for MYCN-mediated repression and for
                      epigenetic silencing of p19-INK4d by DNA hypermethylation in
                      high-risk neuroblastomas.},
      keywords     = {Antimetabolites, Antineoplastic (NLM Chemicals) / CDKN2D
                      protein, human (NLM Chemicals) / Cyclin-Dependent Kinase
                      Inhibitor p19 (NLM Chemicals) / MYCN protein, human (NLM
                      Chemicals) / N-Myc Proto-Oncogene Protein (NLM Chemicals) /
                      Nuclear Proteins (NLM Chemicals) / Oncogene Proteins (NLM
                      Chemicals) / Tretinoin (NLM Chemicals) / decitabine (NLM
                      Chemicals) / Azacitidine (NLM Chemicals)},
      cin          = {C010 / C060 / B062 / B087},
      ddc          = {570},
      cid          = {I:(DE-He78)C010-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)B062-20160331 / I:(DE-He78)B087-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25104850},
      doi          = {10.1093/hmg/ddu406},
      url          = {https://inrepo02.dkfz.de/record/119889},
}