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@ARTICLE{vonKnebelDoeberitz:180028,
      author       = {N. von Knebel Doeberitz$^*$ and D. Paech$^*$ and D.
                      Sturm$^*$ and S. Pusch$^*$ and S. Turcan and Y.
                      Saunthararajah},
      title        = {{C}hanging paradigms in oncology: toward non-cytotoxic
                      treatments for advanced gliomas.},
      journal      = {International journal of cancer},
      volume       = {151},
      number       = {9},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2022-01045},
      pages        = {1431-1446},
      year         = {2022},
      note         = {#EA:E010# / 2022 Nov 1;151(9):1431-1446},
      abstract     = {Glial-lineage malignancies (gliomas) recurrently mutate
                      and/or delete the master regulators of apoptosis p53 and/or
                      p16/CDKN2A, undermining apoptosis-intending (cytotoxic)
                      treatments. By contrast to disrupted p53/p16, glioma cells
                      are live-wired with the master transcription factor circuits
                      that specify and drive glial lineage-fates: these
                      transcription factors activate early-glial and replication
                      programs as expected, but fail in their other usual function
                      of forcing onward glial lineage-maturation - late-glial
                      genes have constitutively 'closed' chromatin requiring
                      chromatin-remodeling for activation - glioma-genesis
                      disrupts several epigenetic components needed to perform
                      this work, and simultaneously amplifies repressing
                      epigenetic machinery instead. Pharmacologic inhibition of
                      repressing epigenetic enzymes thus allows activation of
                      late-glial genes and terminates glioma self-replication
                      (self-replication = replication without lineage-maturation),
                      independent of p53/p16/apoptosis. Lineage-specifying master
                      transcription factors therefore contrast with p53/p16 in
                      being enriched in self-replicating glioma cells, reveal a
                      cause-effect relationship between aberrant epigenetic
                      repression of late-lineage programs and malignant
                      self-replication, and point to specific epigenetic targets
                      for non-cytotoxic glioma-therapy.},
      subtyp        = {Review Article},
      keywords     = {Cancer Epigenetics (Other) / Epigenetic Glioma Therapy
                      (Other) / Glioma (Other) / Glioma Therapy (Other) /
                      Neurooncology (Other)},
      cin          = {E010 / B360 / HD01 / B300 / B062},
      ddc          = {610},
      cid          = {I:(DE-He78)E010-20160331 / I:(DE-He78)B360-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)B300-20160331 /
                      I:(DE-He78)B062-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35603902},
      doi          = {10.1002/ijc.34131},
      url          = {https://inrepo02.dkfz.de/record/180028},
}