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@ARTICLE{ColmeneroRepiso:166277,
      author       = {A. Colmenero-Repiso and M. A. Gómez-Muñoz and I.
                      Rodríguez-Prieto and A. Amador-Álvarez and K.-O.
                      Henrich$^*$ and D. Pascual-Vaca and K. Okonechnikov$^*$ and
                      E. Rivas and F. Westermann$^*$ and R. Pardal and F. M. Vega},
      title        = {{I}dentification of {VRK}1 as a {N}ew {N}euroblastoma
                      {T}umor {P}rogression {M}arker {R}egulating {C}ell
                      {P}roliferation.},
      journal      = {Cancers},
      volume       = {12},
      number       = {11},
      issn         = {2072-6694},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2020-02770},
      pages        = {3465},
      year         = {2020},
      abstract     = {Neuroblastoma (NB) is one of the most common pediatric
                      cancers and presents a poor survival rate in affected
                      children. Current pretreatment risk assessment relies on a
                      few known molecular parameters, like the amplification of
                      the oncogene MYCN. However, a better molecular knowledge
                      about the aggressive progression of the disease is needed to
                      provide new therapeutical targets and prognostic markers and
                      to improve patients' outcomes. The human protein kinase VRK1
                      phosphorylates various signaling molecules and transcription
                      factors to regulate cell cycle progression and other
                      processes in physiological and pathological situations.
                      Using neuroblastoma tumor expression data, tissue
                      microarrays from fresh human samples and patient-derived
                      xenografts (PDXs), we have determined that VRK1 kinase
                      expression stratifies patients according to tumor
                      aggressiveness and survival, allowing the identification of
                      patients with worse outcome among intermediate risk. VRK1
                      associates with cell cycle signaling pathways in NB and its
                      downregulation abrogates cell proliferation in vitro and in
                      vivo. Through the analysis of ChIP-seq and methylation data
                      from NB tumors, we show that VRK1 is a MYCN gene target,
                      however VRK1 correlates with NB aggressiveness independently
                      of MYCN gene amplification, synergizing with the oncogene to
                      drive NB progression. Our study also suggests that VRK1
                      inhibition may constitute a novel cell-cycle-targeted
                      strategy for anticancer therapy in neuroblastoma.},
      keywords     = {MYCN (Other) / VRK1 (Other) / high-risk (Other) /
                      neuroblastoma (Other) / proliferation (Other) /
                      tumorigenesis (Other)},
      cin          = {B062 / B087},
      ddc          = {610},
      cid          = {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:33233777},
      pmc          = {pmc:PMC7699843},
      doi          = {10.3390/cancers12113465},
      url          = {https://inrepo02.dkfz.de/record/166277},
}