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@ARTICLE{Stalmann:178445,
      author       = {U. S. A. Stalmann and F. Ticconi and I. A. M. Snoeren and
                      R. Li and H. Gleitz and G. Cowley and M. E. McConkey and A.
                      B. Wong and S. Schmitz and S. N. R. Fuchs and S. Sood$^*$
                      and N. B. Leimkühler and S. Martinez-Høyer and B. Banjanin
                      and D. E. Root and T. H. Brümmendorf and J. Pearce and A.
                      Schuppert and E. Bindels and M. Essers$^*$ and D. Heckl and
                      T. P. Stiehl and I. G. Costa and B. L. Ebert and R. K.
                      Schneider},
      title        = {{G}enetic barcoding systematically comparing genes in
                      del(5q) {MDS} reveals a central role for {CSNK}1{A}1 in
                      clonal expansion.},
      journal      = {Blood advances},
      volume       = {6},
      number       = {6},
      issn         = {2473-9529},
      address      = {Washington, DC},
      publisher    = {American Society of Hematology},
      reportid     = {DKFZ-2022-00071},
      pages        = {1780-1796},
      year         = {2022},
      note         = {2022 Mar 22;6(6):1780-1796},
      abstract     = {How genetic haploinsufficiency contributes to the clonal
                      dominance of hematopoietic stem cells (HSC) in del(5q)
                      myelodysplastic syndrome (MDS) remains unresolved. Using a
                      genetic barcoding strategy, a systematic comparison was
                      carried out on genes implicated in the pathogenesis of
                      del(5q) MDS in direct competition with each other and
                      wild-type (WT) cells with single clone resolution. Csnk1a1
                      haploinsufficient HSCs expanded (oligo)clonally and
                      outcompeted all other tested genes and combinations.
                      Csnk1a1-/+ multipotent progenitors showed a
                      pro-proliferative gene signature and HSCs a downregulation
                      of inflammatory signaling/immune response. In validation
                      experiments, Csnk1a1-/+ HSCs outperformed their WT
                      counterparts under a chronic inflammation stimulus, also
                      known to be caused by neighboring genes on chromosome 5. A
                      crucial role for Csnk1a1 haploinsufficiency in the selective
                      advantage of the 5q- HSC is therefore proposed. It is
                      implemented by creation of a unique competitive advantage
                      through increased HSC self-renewal and proliferation
                      capacity, as well as increased fitness under inflammatory
                      stress.},
      cin          = {A011 / V960},
      ddc          = {610},
      cid          = {I:(DE-He78)A011-20160331 / I:(DE-He78)V960-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35016204},
      doi          = {10.1182/bloodadvances.2021006061},
      url          = {https://inrepo02.dkfz.de/record/178445},
}