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@ARTICLE{Josupeit:128850,
      author       = {R. Josupeit$^*$ and S. Bender$^*$ and S. Kern$^*$ and B.
                      Leuchs$^*$ and T. Hielscher$^*$ and C. Herold-Mende and J.
                      R. Schlehofer$^*$ and C. Dinsart$^*$ and O. Witt$^*$ and J.
                      Rommelaere$^*$ and J. A. D. Lacroix$^*$},
      title        = {{P}ediatric and {A}dult {H}igh-{G}rade {G}lioma {S}tem
                      {C}ell {C}ulture {M}odels {A}re {P}ermissive to {L}ytic
                      {I}nfection with {P}arvovirus {H}-1.},
      journal      = {Viruses},
      volume       = {8},
      number       = {5},
      issn         = {1999-4915},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2017-04863},
      pages        = {138 -},
      year         = {2016},
      abstract     = {Combining virus-induced cytotoxic and immunotherapeutic
                      effects, oncolytic virotherapy represents a promising
                      therapeutic approach for high-grade glioma (HGG). A clinical
                      trial has recently provided evidence for the clinical safety
                      of the oncolytic parvovirus H-1 (H-1PV) in adult
                      glioblastoma relapse patients. The present study assesses
                      the efficacy of H-1PV in eliminating HGG initiating cells.
                      H-1PV was able to enter and to transduce all HGG neurosphere
                      culture models (n = 6), including cultures derived from
                      adult glioblastoma, pediatric glioblastoma, and diffuse
                      intrinsic pontine glioma. Cytotoxic effects induced by the
                      virus have been observed in all HGG neurospheres at half
                      maximal inhibitory concentration (IC50) doses of input virus
                      between 1 and 10 plaque forming units per cell. H-1PV
                      infection at this dose range was able to prevent
                      tumorigenicity of NCH421k glioblastoma multiforme (GBM)
                      'stem-like' cells in NOD/SCID mice. Interestingly NCH421R,
                      an isogenic subclone with equal capacity of xenograft
                      formation, but resistant to H-1PV infection could be
                      isolated from the parental NCH421k culture. To reveal
                      changes in gene expression associated with H-1PV resistance
                      we performed a comparative gene expression analysis in these
                      subclones. Several dysregulated genes encoding receptor
                      proteins, endocytosis factors or regulators innate antiviral
                      responses were identified and represent intriguing
                      candidates for to further study molecular mechanisms of
                      H-1PV resistance.},
      cin          = {F010 / B062 / C060 / G340},
      ddc          = {610},
      cid          = {I:(DE-He78)F010-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)C060-20160331 / I:(DE-He78)G340-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27213425},
      pmc          = {pmc:PMC4885093},
      doi          = {10.3390/v8050138},
      url          = {https://inrepo02.dkfz.de/record/128850},
}