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@ARTICLE{Mackay:134833,
      author       = {A. Mackay and A. Burford and V. Molinari and D. Jones$^*$
                      and E. Izquierdo and J. Brouwer-Visser and F. Giangaspero
                      and C. Haberler and T. Pietsch and T. S. Jacques and D.
                      Figarella-Branger and D. Rodriguez and P. S. Morgan and P.
                      Raman and A. J. Waanders and A. C. Resnick and M. Massimino
                      and M. L. Garrè and H. Smith and D. Capper$^*$ and S.
                      Pfister$^*$ and T. Würdinger and R. Tam and J. Garcia and
                      M. D. Thakur and G. Vassal and J. Grill and T. Jaspan and P.
                      Varlet and C. Jones},
      title        = {{M}olecular, {P}athological, {R}adiological, and {I}mmune
                      {P}rofiling of {N}on-brainstem {P}ediatric {H}igh-{G}rade
                      {G}lioma from the {HERBY} {P}hase {II} {R}andomized
                      {T}rial.},
      journal      = {Cancer cell},
      volume       = {33},
      number       = {5},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2018-00623},
      pages        = {829 - 842.e5},
      year         = {2018},
      abstract     = {The HERBY trial was a phase II open-label, randomized,
                      multicenter trial evaluating bevacizumab (BEV) in addition
                      to temozolomide/radiotherapy in patients with newly
                      diagnosed non-brainstem high-grade glioma (HGG) between the
                      ages of 3 and 18 years. We carried out comprehensive
                      molecular analysis integrated with pathology, radiology, and
                      immune profiling. In post-hoc subgroup analysis,
                      hypermutator tumors (mismatch repair deficiency and somatic
                      POLE/POLD1 mutations) and those biologically resembling
                      pleomorphic xanthoastrocytoma ([PXA]-like, driven by
                      $BRAF_V600E$ or NF1 mutation) had significantly more CD8+
                      tumor-infiltrating lymphocytes, and longer survival with the
                      addition of BEV. Histone H3 subgroups (hemispheric G34R/V
                      and midline K27M) had a worse outcome and were immune cold.
                      Future clinical trials will need to take into account the
                      diversity represented by the term 'HGG' in the pediatric
                      population.},
      cin          = {B062 / L101 / G380 / L201},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)G380-20160331 / I:(DE-He78)L201-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29763623},
      pmc          = {pmc:PMC5956280},
      doi          = {10.1016/j.ccell.2018.04.004},
      url          = {https://inrepo02.dkfz.de/record/134833},
}