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@ARTICLE{Bloehdorn:172528,
      author       = {J. Bloehdorn and A. Braun and A. Taylor-Weiner and B. M. C.
                      Jebaraj and S. Robrecht and J. Krzykalla$^*$ and H. Pan and
                      A. Giza and G. Akylzhanova and K. Holzmann and A. Scheffold
                      and H. E. Johnston and R.-F. Yeh and T. Klymenko and E.
                      Tausch and B. Eichhorst and L. Bullinger and K. Fischer and
                      M. Weisser and T. Robak and C. Schneider and J. Gribben and
                      L. N. Dahal and M. J. Carter and O. Elemento and D. A.
                      Landau and D. S. Neuberg and M. S. Cragg and A. Benner$^*$
                      and M. Hallek and C. J. Wu and H. Döhner and S.
                      Stilgenbauer and D. Mertens$^*$},
      title        = {{M}ulti-platform profiling characterizes molecular
                      subgroups and resistance networks in chronic lymphocytic
                      leukemia.},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-02076},
      pages        = {5395},
      year         = {2021},
      note         = {#LA:B061#},
      abstract     = {Knowledge of the genomic landscape of chronic lymphocytic
                      leukemia (CLL) grows increasingly detailed, providing
                      challenges in contextualizing the accumulated information.
                      To define the underlying networks, we here perform a
                      multi-platform molecular characterization. We identify major
                      subgroups characterized by genomic instability (GI) or
                      activation of epithelial-mesenchymal-transition (EMT)-like
                      programs, which subdivide into non-inflammatory and
                      inflammatory subtypes. GI CLL exhibit disruption of genome
                      integrity, DNA-damage response and are associated with
                      mutagenesis mediated through activation-induced cytidine
                      deaminase or defective mismatch repair. TP53 wild-type and
                      mutated/deleted cases constitute a transcriptionally uniform
                      entity in GI CLL and show similarly poor progression-free
                      survival at relapse. EMT-like CLL exhibit high genomic
                      stability, reduced benefit from the addition of rituximab
                      and EMT-like differentiation is inhibited by induction of
                      DNA damage. This work extends the perspective on CLL biology
                      and risk categories in TP53 wild-type CLL. Furthermore,
                      molecular targets identified within each subgroup provide
                      opportunities for new treatment approaches.},
      cin          = {C060 / B061},
      ddc          = {500},
      cid          = {I:(DE-He78)C060-20160331 / I:(DE-He78)B061-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34518531},
      pmc          = {pmc:PMC8438057},
      doi          = {10.1038/s41467-021-25403-y},
      url          = {https://inrepo02.dkfz.de/record/172528},
}