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@ARTICLE{Mardin:127064,
      author       = {B. R. Mardin and A. P. Drainas and S. M. Waszak and J.
                      Weischenfeldt and M. Isokane and A. M. Stütz and B. Raeder
                      and T. Efthymiopoulos and C. Buccitelli and M. Segura-Wang
                      and P. Northcott$^*$ and S. Pfister$^*$ and P. Lichter and
                      J. Ellenberg and J. O. Korbel},
      title        = {{A} cell-based model system links chromothripsis with
                      hyperploidy.},
      journal      = {Molecular systems biology},
      volume       = {11},
      number       = {9},
      issn         = {1744-4292},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DKFZ-2017-03090},
      pages        = {828},
      year         = {2015},
      abstract     = {A remarkable observation emerging from recent cancer genome
                      analyses is the identification of chromothripsis as a
                      one-off genomic catastrophe, resulting in massive somatic
                      DNA structural rearrangements (SRs). Largely due to lack of
                      suitable model systems, the mechanistic basis of
                      chromothripsis has remained elusive. We developed an
                      integrative method termed 'complex alterations after
                      selection and transformation (CAST),' enabling efficient in
                      vitro generation of complex DNA rearrangements including
                      chromothripsis, using cell perturbations coupled with a
                      strong selection barrier followed by massively parallel
                      sequencing. We employed this methodology to characterize
                      catastrophic SR formation processes, their temporal
                      sequence, and their impact on gene expression and cell
                      division. Our in vitro system uncovered a propensity of
                      chromothripsis to occur in cells with damaged telomeres, and
                      in particular in hyperploid cells. Analysis of primary
                      medulloblastoma cancer genomes verified the link between
                      hyperploidy and chromothripsis in vivo. CAST provides the
                      foundation for mechanistic dissection of complex DNA
                      rearrangement processes.},
      keywords     = {Telomeric Repeat Binding Protein 2 (NLM Chemicals)},
      cin          = {B062 / B060},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B060-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26415501},
      pmc          = {pmc:PMC4592670},
      url          = {https://inrepo02.dkfz.de/record/127064},
}