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@ARTICLE{Man:293327,
      author       = {K. H. Man$^*$ and Y. Wu and Z. Gao and A.-S. Spreng$^*$ and
                      S. J. E. Keding$^*$ and J. Mangei$^*$ and P. Boskovic$^*$
                      and J.-P. Mallm$^*$ and H.-K. Liu$^*$ and C. D. Imbusch$^*$
                      and P. Lichter$^*$ and B. Radlwimmer$^*$},
      title        = {{SOX}10 mediates glioblastoma cell-state plasticity.},
      journal      = {EMBO reports},
      volume       = {25},
      number       = {11},
      issn         = {1469-221X},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2024-01877},
      pages        = {5113-5140},
      year         = {2024},
      note         = {#EA:B060#LA:B060# / 2024 Nov;25(11):5113-5140},
      abstract     = {Phenotypic plasticity is a cause of glioblastoma therapy
                      failure. We previously showed that suppressing the
                      oligodendrocyte-lineage regulator SOX10 promotes
                      glioblastoma progression. Here, we analyze SOX10-mediated
                      phenotypic plasticity and exploit it for glioblastoma
                      therapy design. We show that low SOX10 expression is linked
                      to neural stem-cell (NSC)-like glioblastoma cell states and
                      is a consequence of temozolomide treatment in animal and
                      cell line models. Single-cell transcriptome profiling of
                      Sox10-KD tumors indicates that Sox10 suppression is
                      sufficient to induce tumor progression to an aggressive
                      NSC/developmental-like phenotype, including a quiescent
                      NSC-like cell population. The quiescent NSC state is induced
                      by temozolomide and Sox10-KD and reduced by Notch pathway
                      inhibition in cell line models. Combination treatment using
                      Notch and HDAC/PI3K inhibitors extends the survival of mice
                      carrying Sox10-KD tumors, validating our experimental
                      therapy approach. In summary, SOX10 suppression mediates
                      glioblastoma progression through NSC/developmental
                      cell-state transition, including the induction of a
                      targetable quiescent NSC state. This work provides a
                      rationale for the design of tumor therapies based on
                      single-cell phenotypic plasticity analysis.},
      keywords     = {SOX10 (Other) / Glioblastoma (Other) / Phenotypic
                      Plasticity (Other) / Therapy Resistance (Other) / Tumor Cell
                      Quiescence (Other)},
      cin          = {B060 / B330 / A240 / W192},
      ddc          = {570},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)B330-20160331 /
                      I:(DE-He78)A240-20160331 / I:(DE-He78)W192-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39285246},
      doi          = {10.1038/s44319-024-00258-8},
      url          = {https://inrepo02.dkfz.de/record/293327},
}