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@ARTICLE{Giessler:125202,
      author       = {K. Giessler$^*$ and K. Kleinheinz$^*$ and D.
                      Huebschmann$^*$ and G. P. Balasubramanian$^*$ and T. D.
                      Dubash$^*$ and S. M. Dieter$^*$ and C. Siegl$^*$ and F.
                      Herbst$^*$ and S. Weber$^*$ and C. M. Hoffmann and R.
                      Fronza$^*$ and I. Buchhalter$^*$ and N. Paramasivam$^*$ and
                      R. Eils$^*$ and M. Schmidt$^*$ and C. von Kalle$^*$ and M.
                      Schneider and A. Ulrich and C. Scholl$^*$ and S.
                      Fröhling$^*$ and W. Weichert$^*$ and B. Brors$^*$ and M.
                      Schlesner$^*$ and C. R. Ball$^*$ and H. Glimm$^*$},
      title        = {{G}enetic subclone architecture of tumor clone-initiating
                      cells in colorectal cancer.},
      journal      = {Journal of experimental medicine},
      volume       = {214},
      number       = {7},
      issn         = {1540-9538},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DKFZ-2017-01357},
      pages        = {2073 - 2088},
      year         = {2017},
      abstract     = {A hierarchically organized cell compartment drives
                      colorectal cancer (CRC) progression. Genetic barcoding
                      allows monitoring of the clonal output of tumorigenic cells
                      without prospective isolation. In this study, we asked
                      whether tumor clone-initiating cells (TcICs) were
                      genetically heterogeneous and whether differences in
                      self-renewal and activation reflected differential kinetics
                      among individual subclones or functional hierarchies within
                      subclones. Monitoring genomic subclone kinetics in three
                      patient tumors and corresponding serial xenografts and
                      spheroids by high-coverage whole-genome sequencing,
                      clustering of genetic aberrations, subclone combinatorics,
                      and mutational signature analysis revealed at least two to
                      four genetic subclones per sample. Long-term growth in
                      serial xenografts and spheroids was driven by multiple
                      genomic subclones with profoundly differing growth dynamics
                      and hence different quantitative contributions over time.
                      Strikingly, genetic barcoding demonstrated stable functional
                      heterogeneity of CRC TcICs during serial xenografting
                      despite near-complete changes in genomic subclone
                      contribution. This demonstrates that functional
                      heterogeneity is, at least frequently, present within
                      genomic subclones and independent of mutational subclone
                      differences.},
      cin          = {B080 / G100 / G200 / G102 / L101 / L701},
      ddc          = {610},
      cid          = {I:(DE-He78)B080-20160331 / I:(DE-He78)G100-20160331 /
                      I:(DE-He78)G200-20160331 / I:(DE-He78)G102-20160331 /
                      I:(DE-He78)L101-20160331 / I:(DE-He78)L701-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28572216},
      pmc          = {pmc:PMC5502434},
      doi          = {10.1084/jem.20162017},
      url          = {https://inrepo02.dkfz.de/record/125202},
}