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@ARTICLE{Fisher:167470,
      author       = {M. J. Fisher and D. T. W. Jones$^*$ and Y. Li and X. Guo
                      and P. S. Sonawane and A. J. Waanders and J. J. Phillips and
                      W. A. Weiss and A. C. Resnick and S. Gosline and J. Banerjee
                      and J. Guinney and A. Gnekow and D. Kandels and N. K.
                      Foreman and A. Korshunov and M. Ryzhova and L. Massimi and
                      S. Gururangan and M. W. Kieran and Z. Wang and M. Fouladi
                      and M. Sato and I. Øra and S. Holm and S. J. Markham and P.
                      Beck$^*$ and N. Jäger$^*$ and A. Wittmann$^*$ and A. C.
                      Sommerkamp$^*$ and F. Sahm and S. Pfister$^*$ and D. H.
                      Gutmann},
      title        = {{I}ntegrated molecular and clinical analysis of low-grade
                      gliomas in children with neurofibromatosis type 1 ({NF}1).},
      journal      = {Acta neuropathologica},
      volume       = {141},
      number       = {4},
      issn         = {0001-6322},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DKFZ-2021-00373},
      pages        = {605-617},
      year         = {2021},
      note         = {2021 Apr;141(4):605-617 / #EA:B360#LA:B062#},
      abstract     = {Low-grade gliomas (LGGs) are the most common childhood
                      brain tumor in the general population and in individuals
                      with the Neurofibromatosis type 1 (NF1) cancer
                      predisposition syndrome. Surgical biopsy is rarely performed
                      prior to treatment in the setting of NF1, resulting in a
                      paucity of tumor genomic information. To define the
                      molecular landscape of NF1-associated LGGs (NF1-LGG), we
                      integrated clinical data, histological diagnoses, and
                      multi-level genetic/genomic analyses on 70 individuals from
                      25 centers worldwide. Whereas, most tumors harbored
                      bi-allelic NF1 inactivation as the only genetic abnormality,
                      $11\%$ had additional mutations. Moreover, tumors classified
                      as non-pilocytic astrocytoma based on DNA methylation
                      analysis were significantly more likely to harbor these
                      additional mutations. The most common secondary alteration
                      was FGFR1 mutation, which conferred an additional growth
                      advantage in multiple complementary experimental murine Nf1
                      models. Taken together, this comprehensive characterization
                      has important implications for the management of children
                      with NF1-LGG, distinct from their sporadic counterparts.},
      keywords     = {FGFR1 (Other) / Methylation (Other) / Neurofibromatosis
                      (Other) / Pediatric brain tumor (Other) / Pilocytic
                      astrocytoma (Other)},
      cin          = {B360 / B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B360-20160331 / I:(DE-He78)B062-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33585982},
      doi          = {10.1007/s00401-021-02276-5.},
      url          = {https://inrepo02.dkfz.de/record/167470},
}