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@ARTICLE{Collins:126279,
      author       = {V. P. Collins and D. Jones$^*$ and C. Giannini},
      title        = {{P}ilocytic astrocytoma: pathology, molecular mechanisms
                      and markers.},
      journal      = {Acta neuropathologica},
      volume       = {129},
      number       = {6},
      issn         = {1432-0533},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {DKFZ-2017-02394},
      pages        = {775 - 788},
      year         = {2015},
      abstract     = {Pilocytic astrocytomas (PAs) were recognized as a discrete
                      clinical entity over 70 years ago. They are relatively
                      benign (WHO grade I) and have, as a group, a 10-year
                      survival of over $90\%.$ Many require merely surgical
                      removal and only very infrequently do they progress to more
                      malignant gliomas. While most show classical morphology,
                      they may present a spectrum of morphological patterns, and
                      there are difficult cases that show similarities to other
                      gliomas, some of which are malignant and require aggressive
                      treatment. Until recently, almost nothing was known about
                      the molecular mechanisms involved in their development. The
                      use of high-throughput sequencing techniques interrogating
                      the whole genome has shown that single abnormalities of the
                      mitogen-activating protein kinase (MAPK) pathway are
                      exclusively found in almost all cases, indicating that PA
                      represents a one-pathway disease. The most common mechanism
                      is a tandem duplication of a ≈2 Mb-fragment of #7q, giving
                      rise to a fusion between two genes, resulting in a
                      transforming fusion protein, consisting of the N-terminus of
                      KIAA1549 and the kinase domain of BRAF. Additional
                      infrequent fusion partners have been identified, along with
                      other abnormalities of the MAP-K pathway, affecting tyrosine
                      kinase growth factor receptors at the cell surface (e.g.,
                      FGFR1) as well as BRAF V600E, KRAS, and NF1 mutations among
                      others. However, while the KIAA1549-BRAF fusion occurs in
                      all areas, the incidence of the various other mutations
                      identified differs in PAs that develop in different regions
                      of the brain. Unfortunately, from a diagnostic standpoint,
                      almost all mutations found have been reported in other brain
                      tumor types, although some retain considerable utility.
                      These molecular abnormalities will be reviewed, and the
                      difficulties in their potential use in supporting a
                      diagnosis of PA, when the histopathological findings are
                      equivocal or in the choice of individualized therapy, will
                      be discussed.},
      cin          = {B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25792358},
      pmc          = {pmc:PMC4436848},
      doi          = {10.1007/s00401-015-1410-7},
      url          = {https://inrepo02.dkfz.de/record/126279},
}