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@ARTICLE{Vu:156883,
      author       = {T. Vu and J. Straube and A. H. Porter and M. Bywater and A.
                      Song and V. Ling and L. Cooper and G. Pali and C. Bruedigam
                      and S. Jacquelin and J. Green and G. Magor and A. Perkins
                      and A. M. Chalk and C. R. Walkley and F. H. Heidel and P.
                      Mukhopadhyay and N. Cloonan and S. Gröschel$^*$ and J.-P.
                      Mallm$^*$ and S. Fröhling$^*$ and C. Scholl$^*$ and S. W.
                      Lane},
      title        = {{H}ematopoietic stem and progenitor cell-restricted {C}dx2
                      expression induces transformation to myelodysplasia and
                      acute leukemia.},
      journal      = {Nature Communications},
      volume       = {11},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2020-01190},
      pages        = {3021},
      year         = {2020},
      abstract     = {The caudal-related homeobox transcription factor CDX2 is
                      expressed in leukemic cells but not during normal blood
                      formation. Retroviral overexpression of Cdx2 induces AML in
                      mice, however the developmental stage at which CDX2 exerts
                      its effect is unknown. We developed a conditionally
                      inducible Cdx2 mouse model to determine the effects of in
                      vivo, inducible Cdx2 expression in hematopoietic stem and
                      progenitor cells (HSPCs). Cdx2-transgenic mice develop
                      myelodysplastic syndrome with progression to acute leukemia
                      associated with acquisition of additional driver mutations.
                      Cdx2-expressing HSPCs demonstrate enrichment of
                      hematopoietic-specific enhancers associated with
                      pro-differentiation transcription factors. Furthermore,
                      treatment of Cdx2 AML with azacitidine decreases leukemic
                      burden. Extended scheduling of low-dose azacitidine shows
                      greater efficacy in comparison to intermittent higher-dose
                      azacitidine, linked to more specific epigenetic modulation.
                      Conditional Cdx2 expression in HSPCs is an inducible model
                      of de novo leukemic transformation and can be used to
                      optimize treatment in high-risk AML.},
      cin          = {A380 / B066 / W192 / B340 / B290},
      ddc          = {500},
      cid          = {I:(DE-He78)A380-20160331 / I:(DE-He78)B066-20160331 /
                      I:(DE-He78)W192-20160331 / I:(DE-He78)B340-20160331 /
                      I:(DE-He78)B290-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32541670},
      pmc          = {pmc:PMC7296000},
      doi          = {10.1038/s41467-020-16840-2},
      url          = {https://inrepo02.dkfz.de/record/156883},
}