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@ARTICLE{Schipper:128262,
      author       = {H. Schipper and V. Alla and C. Meier and D. Nettelbeck$^*$
                      and O. Herchenröder and B. M. Pützer},
      title        = {{E}radication of metastatic melanoma through cooperative
                      expression of {RNA}-based {HDAC}1 inhibitor and p73 by
                      oncolytic adenovirus.},
      journal      = {OncoTarget},
      volume       = {5},
      number       = {15},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-04279},
      pages        = {5893 - 5907},
      year         = {2014},
      abstract     = {Malignant melanoma is a highly aggressive cancer that
                      retains functional p53 and p73, and drug unresponsiveness
                      largely depends on defects in death pathways after
                      epigenetic gene silencing in conjunction with an imbalanced
                      p73/DNp73 ratio. We constructed oncolytic viruses armed with
                      an inhibitor of deacetylation and/or p73 to specifically
                      target metastatic cancer. Arming of the viruses is aimed at
                      lifting epigenetic blockage and re-opening apoptotic
                      programs in a staggered manner enabling both, efficient
                      virus replication and balanced destruction of target cells
                      through apoptosis. Our results showed that cooperative
                      expression of shHDAC1 and p73 efficiently enhances apoptosis
                      induction and autophagy of infected cells which reinforces
                      progeny production. In vitro analyses revealed $100\%$
                      cytotoxicity after infecting cells with OV.shHDAC1.p73 at a
                      lower virus dose compared to control viruses. Intriguingly,
                      OV.shHDAC1.p73 acts as a potent inhibitor of highly
                      metastatic xenograft tumors in vivo. Tumor expansion was
                      significantly reduced after intratumoral injection of 3 x
                      10⁸ PFU of either OV.shHDAC1 or OV.p73 and, most
                      important, complete regression could be achieved in 100 $\%$
                      of tumors treated with OV.shHDAC1.p73. Our results point out
                      that the combination of high replication capacity and
                      simultaneous restoration of cell death routes significantly
                      enhance antitumor activity.},
      keywords     = {DNA-Binding Proteins (NLM Chemicals) / Nuclear Proteins
                      (NLM Chemicals) / RNA, Small Interfering (NLM Chemicals) /
                      Tumor Protein p73 (NLM Chemicals) / Tumor Suppressor
                      Proteins (NLM Chemicals) / p73 protein, human (NLM
                      Chemicals) / HDAC1 protein, human (NLM Chemicals) / Histone
                      Deacetylase 1 (NLM Chemicals)},
      cin          = {F110},
      ddc          = {610},
      cid          = {I:(DE-He78)F110-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25071017},
      pmc          = {pmc:PMC4171600},
      doi          = {10.18632/oncotarget.1839},
      url          = {https://inrepo02.dkfz.de/record/128262},
}