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@ARTICLE{Young:169353,
      author       = {M. D. Young and T. J. Mitchell and L. Custers and T.
                      Margaritis and F. Morales-Rodriguez and K. Kwakwa and E.
                      Khabirova and G. Kildisiute and T. R. W. Oliver and R. R. de
                      Krijger and M. M. van den Heuvel-Eibrink and F. Comitani and
                      A. Piapi and E. Bugallo-Blanco and C. Thevanesan and C.
                      Burke and E. Prigmore and K. Ambridge and K. Roberts and F.
                      A. V. Braga and T. H. H. Coorens and I. Del Valle and A.
                      Wilbrey-Clark and L. Mamanova and G. D. Stewart and V. J.
                      Gnanapragasam and D. Rampling and N. Sebire and N. Coleman
                      and L. Hook and A. Warren and M. Haniffa and M. Kool$^*$ and
                      S. M. Pfister$^*$ and J. C. Achermann and X. He and R. A.
                      Barker and A. Shlien and O. A. Bayraktar and S. A. Teichmann
                      and F. C. Holstege and K. B. Meyer and J. Drost and K.
                      Straathof and S. Behjati},
      title        = {{S}ingle cell derived m{RNA} signals across human kidney
                      tumors.},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-01433},
      pages        = {3896},
      year         = {2021},
      abstract     = {Tumor cells may share some patterns of gene expression with
                      their cell of origin, providing clues into the
                      differentiation state and origin of cancer. Here, we study
                      the differentiation state and cellular origin of 1300
                      childhood and adult kidney tumors. Using single cell mRNA
                      reference maps of normal tissues, we quantify reference
                      'cellular signals' in each tumor. Quantifying global
                      differentiation, we find that childhood tumors exhibit fetal
                      cellular signals, replacing the presumption of 'fetalness'
                      with a quantitative measure of immaturity. By contrast, in
                      adult cancers our assessment refutes the suggestion of
                      dedifferentiation towards a fetal state in most cases. We
                      find an intimate connection between developmental
                      mesenchymal populations and childhood renal tumors. We
                      demonstrate the diagnostic potential of our approach with a
                      case study of a cryptic renal tumor. Our findings provide a
                      cellular definition of human renal tumors through an
                      approach that is broadly applicable to human cancer.},
      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:34162837},
      doi          = {10.1038/s41467-021-23949-5},
      url          = {https://inrepo02.dkfz.de/record/169353},
}