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@ARTICLE{Custers:167780,
      author       = {L. Custers and E. Khabirova and T. H. H. Coorens and T. R.
                      W. Oliver and C. Calandrini and M. D. Young and F. A. Vieira
                      Braga and P. Ellis and L. Mamanova and H. Segers and A. Maat
                      and M. Kool$^*$ and E. W. Hoving and M. M. van den
                      Heuvel-Eibrink and J. Nicholson and K. Straathof and L. Hook
                      and R. R. de Krijger and C. Trayers and K. Allinson and S.
                      Behjati and J. Drost},
      title        = {{S}omatic mutations and single-cell transcriptomes reveal
                      the root of malignant rhabdoid tumours.},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-00542},
      pages        = {1407},
      year         = {2021},
      abstract     = {Malignant rhabdoid tumour (MRT) is an often lethal
                      childhood cancer that, like many paediatric tumours, is
                      thought to arise from aberrant fetal development. The
                      embryonic root and differentiation pathways underpinning MRT
                      are not firmly established. Here, we study the origin of MRT
                      by combining phylogenetic analyses and single-cell mRNA
                      studies in patient-derived organoids. Comparison of somatic
                      mutations shared between cancer and surrounding normal
                      tissues places MRT in a lineage with neural crest-derived
                      Schwann cells. Single-cell mRNA readouts of MRT
                      differentiation, which we examine by reverting the genetic
                      driver mutation underpinning MRT, SMARCB1 loss, suggest that
                      cells are blocked en route to differentiating into
                      mesenchyme. Quantitative transcriptional predictions
                      indicate that combined HDAC and mTOR inhibition mimic MRT
                      differentiation, which we confirm experimentally. Our study
                      defines the developmental block of MRT and reveals potential
                      differentiation therapies.},
      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:33658498},
      doi          = {10.1038/s41467-021-21675-6},
      url          = {https://inrepo02.dkfz.de/record/167780},
}