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@ARTICLE{Ceccon:844885,
      author       = {Ceccon, Garry and Werner, Jan-Michael and Dunkl, Veronika
                      and Tscherpel, Caroline and Stoffels, Gabriele and Brunn,
                      Anna and Deckert, Martina and Fink, Gereon Rudolf and
                      Galldiks, Norbert},
      title        = {{D}abrafenib {T}reatment in a {P}atient with an
                      {E}pithelioid {G}lioblastoma and {BRAF} {V}600{E}
                      {M}utation},
      journal      = {International journal of molecular sciences},
      volume       = {19},
      number       = {4},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {FZJ-2018-02231},
      pages        = {1090 -},
      year         = {2018},
      abstract     = {Novel therapeutic targets in malignant glioma patients are
                      urgently needed. Point mutations of the v-Raf murine sarcoma
                      viral oncogene homolog B (BRAF) gene occur predominantly in
                      melanoma patients, but may also occur in gliomas. Thus, this
                      is a target of great interest for this group of patients. In
                      a nine-year-old male patient, an anaplastic astrocytoma in
                      the left temporoparietal region was diagnosed
                      histologically. After first- and second-line treatment, a
                      malignant progression to a secondary glioblastoma was
                      observed ten years after the initial diagnosis. Within the
                      following seven years, all other conventional treatment
                      options were exhausted. At this time point, recurrent tumor
                      histology revealed an epithelioid glioblastoma, without a
                      mutation in the isocitrate dehydrogenase gene (IDH
                      wild-type). In order to identify a potential target for an
                      experimental salvage therapy, mutational tumor analysis
                      showed a BRAF V600E mutation. Consecutively, dabrafenib
                      treatment was initiated. The patient remained clinically
                      stable, and follow-up magnetic resonance images (MRI) were
                      consistent with “Stable Disease” according to the
                      Response Assessment in Neuro-Oncology Working Group (RANO)
                      criteria for the following ten months until tumor
                      progression was detected. The patient died 16 months after
                      dabrafenib treatment initiation. Particularly in younger
                      glioma patients as well as in patients with an epithelioid
                      glioblastoma, screening for a V600E BRAF mutation is
                      promising since, in these cases, targeted therapy with BRAF
                      inhibitors seems to be a useful salvage treatment option.},
      cin          = {INM-3 / INM-4},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-4-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29621181},
      UT           = {WOS:000434978700169},
      doi          = {10.3390/ijms19041090},
      url          = {https://juser.fz-juelich.de/record/844885},
}