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@ARTICLE{Park:144028,
      author       = {A. K. Park and J. Y. Lee and H. Cheong and V. Ramaswamy and
                      S.-H. Park and M. Kool$^*$ and J. H. Phi and S. A. Choi and
                      F. Cavalli and M. D. Taylor and S.-K. Kim},
      title        = {{S}ubgroup-specific prognostic signaling and metabolic
                      pathways in pediatric medulloblastoma.},
      journal      = {BMC cancer},
      volume       = {19},
      number       = {1},
      issn         = {1471-2407},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DKFZ-2019-01579},
      pages        = {571},
      year         = {2019},
      abstract     = {Using a pathway-focused approach, we aimed to provide a
                      subgroup-specific basis for finding novel therapeutic
                      strategies and further refinement of the risk stratification
                      in pediatric medulloblastoma.Based on genome-wide Cox
                      regression and Gene Set Enrichment Analysis, we investigated
                      prognosis-related signaling pathways and core genes in
                      pediatric medulloblastoma subgroups using 530 patient data
                      from Medulloblastoma Advanced Genomic International
                      Consortium (MAGIC) project. We further examined the
                      relationship between expression of the prognostic core genes
                      and frequent chromosome aberrations using broad range copy
                      number change data.In SHH subgroup, relatively high
                      expression of the core genes involved in p53, PLK1, FOXM1,
                      and Aurora B signaling pathways are associated with poor
                      prognosis, and their average expression synergistically
                      increases with co-occurrence of losses of 17p, 14q, or 10q,
                      or gain of 17q. In Group 3, in addition to high MYC
                      expression, relatively elevated expression of PDGFRA, IGF1R,
                      and FGF2 and their downstream genes in PI3K/AKT and MAPK/ERK
                      pathways are related to poor survival outcome, and their
                      average expression is increased with the presence of
                      isochromosome 17q [i(17q)] and synergistically
                      down-regulated with simultaneous losses of 16p, 8q, or 4q.
                      In Group 4, up-regulation of the genes encoding various
                      immune receptors and those involved in NOTCH, NF-κB,
                      PI3K/AKT, or RHOA signaling pathways are associated with
                      worse prognosis. Additionally, the expressions of Notch
                      genes correlate with those of the prognostic immune
                      receptors. Besides the Group 4 patients with previously
                      known prognostic aberration, loss of chromosome 11, those
                      with loss of 8q but without i(17q) show excellent survival
                      outcomes and low average expression of the prognostic core
                      genes whereas those harboring 10q loss, 1q gain, or 12q gain
                      accompanied by i(17q) show bad outcomes. Finally, several
                      metabolic pathways known to be reprogrammed in cancer cells
                      are detected as prognostic pathways including glutamate
                      metabolism in SHH subgroup, pentose phosphate pathway and
                      TCA cycle in Group 3, and folate-mediated one
                      carbon-metabolism in Group 4.The results underscore several
                      subgroup-specific pathways for potential therapeutic
                      interventions: SHH-GLI-FOXM1 pathway in SHH subgroup,
                      receptor tyrosine kinases and their downstream pathways in
                      Group 3, and immune and inflammatory pathways in Group 4.},
      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:31185958},
      pmc          = {pmc:PMC6560914},
      doi          = {10.1186/s12885-019-5742-x},
      url          = {https://inrepo02.dkfz.de/record/144028},
}