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@ARTICLE{Shiraishi:290623,
      author       = {R. Shiraishi and G. Cancila and K. Kumegawa and J. Torrejon
                      and I. Basili and F. Bernardi and P. B. G. d. Silva$^*$ and
                      W. Wang and O. Chapman and L. Yang and M. Jami and K.
                      Nishitani and Y. Arai and Z. Xiao and H. Yu and V. Lo Re and
                      V. Marsaud and J. Talbot and B. Lombard and D. Loew and M.
                      Jingu and K. Okonechnikov$^*$ and M. Sone and N. Motohashi
                      and Y. Aoki and S. M. Pfister$^*$ and L. Chavez and M.
                      Hoshino and R. Maruyama and O. Ayrault and D. Kawauchi},
      title        = {{C}ancer-specific epigenome identifies oncogenic hijacking
                      by nuclear factor {I} family proteins for medulloblastoma
                      progression.},
      journal      = {Developmental cell},
      volume       = {59},
      number       = {17},
      issn         = {1534-5807},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-01209},
      pages        = {2302-2319.e12},
      year         = {2024},
      note         = {2024 Sep 9;59(17):2302-2319.e12},
      abstract     = {Normal cells coordinate proliferation and differentiation
                      by precise tuning of gene expression based on the dynamic
                      shifts of the epigenome throughout the developmental
                      timeline. Although non-mutational epigenetic reprogramming
                      is an emerging hallmark of cancer, the epigenomic shifts
                      that occur during the transition from normal to malignant
                      cells remain elusive. Here, we capture the epigenomic
                      changes that occur during tumorigenesis in a prototypic
                      embryonal brain tumor, medulloblastoma. By comparing the
                      epigenomes of the different stages of transforming cells in
                      mice, we identify nuclear factor I family of transcription
                      factors, known to be cell fate determinants in development,
                      as oncogenic regulators in the epigenomes of precancerous
                      and cancerous cells. Furthermore, genetic and
                      pharmacological inhibition of NFIB validated a crucial role
                      of this transcription factor by disrupting the cancer
                      epigenome in medulloblastoma. Thus, this study exemplifies
                      how epigenomic changes contribute to tumorigenesis via
                      non-mutational mechanisms involving developmental
                      transcription factors.},
      keywords     = {brain tumor (Other) / cerebellar granule cell (Other) /
                      cerebellum (Other) / epigenome (Other) / medulloblastoma
                      (Other) / mouse model (Other) / nuclear factor I (Other)},
      cin          = {B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38834071},
      doi          = {10.1016/j.devcel.2024.05.013},
      url          = {https://inrepo02.dkfz.de/record/290623},
}