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@ARTICLE{Graf:179252,
      author       = {M. Graf and M. Interlandi and N. Moreno and D. Holdhof and
                      C. Göbel and V. Melcher and J. Mertins and T. K. Albert and
                      D. Kastrati and A. Alfert and T. Holsten and F. de Faria and
                      M. Meisterernst and C. Rossig and M. Warmuth-Metz and J.
                      Nowak and G. Meyer Zu Hörste and C. Mayère and S. Nef and
                      P. Johann$^*$ and M. C. Frühwald and M. Dugas and U.
                      Schüller and K. Kerl},
      title        = {{S}ingle-cell transcriptomics identifies potential cells of
                      origin of {MYC} rhabdoid tumors.},
      journal      = {Nature Communications},
      volume       = {13},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2022-00534},
      pages        = {1544},
      year         = {2022},
      abstract     = {Rhabdoid tumors (RT) are rare and highly aggressive
                      pediatric neoplasms. Their epigenetically-driven
                      intertumoral heterogeneity is well described; however, the
                      cellular origin of RT remains an enigma. Here, we establish
                      and characterize different genetically engineered mouse
                      models driven under the control of distinct promoters and
                      being active in early progenitor cell types with diverse
                      embryonic onsets. From all models only Sox2-positive
                      progenitor cells give rise to murine RT. Using single-cell
                      analyses, we identify distinct cells of origin for the SHH
                      and MYC subgroups of RT, rooting in early stages of
                      embryogenesis. Intra- and extracranial MYC tumors harbor
                      common genetic programs and potentially originate from fetal
                      primordial germ cells (PGCs). Using PGC specific Smarcb1
                      knockout mouse models we validate that MYC RT originate from
                      these progenitor cells. We uncover an epigenetic imbalance
                      in MYC tumors compared to PGCs being sustained by
                      epigenetically-driven subpopulations. Importantly,
                      treatments with the DNA demethylating agent decitabine
                      successfully impair tumor growth in vitro and in vivo. In
                      summary, our work sheds light on the origin of RT and
                      supports the clinical relevance of DNA methyltransferase
                      inhibitors against this disease.},
      cin          = {B062 / HD01},
      ddc          = {500},
      cid          = {I:(DE-He78)B062-20160331 / 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:35318328},
      doi          = {10.1038/s41467-022-29152-4},
      url          = {https://inrepo02.dkfz.de/record/179252},
}