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@ARTICLE{Wang:301504,
      author       = {W. Wang and K. Kumegawa and O. S. Chapman and R. Shiraishi
                      and Z. Xiao and K. Okonechnikov$^*$ and Y. Sun and S. M.
                      Pfister$^*$ and W. Feng and N. Uesaka and M. Hoshino and S.
                      Takahashi and A. Korshunov$^*$ and L. Chavez and R. Maruyama
                      and D. Kawauchi},
      title        = {{C}hromatin modification abnormalities by {CHD}7 and
                      {KMT}2{C} loss promote medulloblastoma progression.},
      journal      = {Cell reports},
      volume       = {44},
      number       = {5},
      issn         = {2211-1247},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2025-01043},
      pages        = {115673},
      year         = {2025},
      note         = {Volume 44, Issue 5, 27 May 2025, 115673},
      abstract     = {Medulloblastoma (MB), a common malignant pediatric brain
                      tumor arising in the cerebellum, is characterized by
                      mutations in chromatin modifiers, highlighting the
                      significance of chromatin modification abnormalities in its
                      progression. While animal models have effectively
                      demonstrated this, a comprehensive evaluation of the
                      oncogenic potential of these mutations remains incomplete.
                      In this study, we use CRISPR-mediated gene editing to knock
                      out chromatin modifier genes mutated in human SHH MB, along
                      with the Ptch1 gene, in cerebellar granule neuron
                      progenitors of neonatal mice. This reveals that depletion of
                      Chd7 and Kmt2c accelerates tumor growth. Multi-layered omics
                      analysis uncovers that inhibition of the neuronal
                      differentiation program by chromatin dysregulation is a key
                      signaling pathway in tumor progression. Additionally, forced
                      expression of Neurod1, a common target of these chromatin
                      modifiers, inhibits proliferation and promotes
                      differentiation. These findings highlight converging
                      chromatin modification abnormalities from distinct mutations
                      in Sonic Hedgehog MB and suggest that epigenetic drugs
                      activating neuronal genes have significant potential as
                      novel treatments.},
      keywords     = {CHD7 (Other) / CP: Cancer (Other) / KMT2C (Other) / brain
                      tumor (Other) / chromatin modifications (Other) /
                      medulloblastoma (Other) / mouse model (Other)},
      cin          = {B062 / B300 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B300-20160331 /
                      I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40393452},
      doi          = {10.1016/j.celrep.2025.115673},
      url          = {https://inrepo02.dkfz.de/record/301504},
}