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@ARTICLE{Hartmann:306830,
      author       = {M. Hartmann$^*$ and M. Schönung$^*$ and J. Rajak and V.
                      Maurer$^*$ and L. Hai$^*$ and K. Bauer$^*$ and M.
                      Hakobyan$^*$ and S. Stäble$^*$ and J. Langstein$^*$ and L.
                      Jardine and R. Roelz and S. Bohler and E. Khabirova and
                      A.-H. Maag and D. Vonficht$^*$ and D. Lebrecht and K. M.
                      Bernt and K. Tan and C. Chen and F. Alikarami and J. Meyer
                      and J. Wang and T. Boch and N. V. Flore$^*$ and P.
                      Lutsik$^*$ and M. Milsom$^*$ and S. Raffel and C. Buske and
                      S. Haas and M. Haniffa and J.-P. Mallm$^*$ and S. Behjati
                      and M. J. Bonder$^*$ and S. Fröhling$^*$ and E. Stieglitz
                      and C. M. Niemeyer and J. Hey$^*$ and C. Flotho$^*$ and C.
                      Plass$^*$ and M. Erlacher$^*$ and M. Schlesner$^*$ and D.
                      Lipka$^*$},
      title        = {{M}olecular {P}lasticity {R}esults in {O}ncofetal
                      {R}eprogramming and {T}herapeutic {V}ulnerabilities in
                      {J}uvenile {M}yelomonocytic {L}eukemia.},
      journal      = {Blood cancer discovery},
      volume       = {nn},
      issn         = {2643-3230},
      address      = {Philadelphia, PA},
      publisher    = {American Association for Cancer Research},
      reportid     = {DKFZ-2025-02807},
      pages        = {nn},
      year         = {2025},
      note         = {DKFZ-ZMBH Alliance/ #EA:B340#LA:B340#LA:B370#LA:W610# /
                      epub},
      abstract     = {Persistent fetal gene expression in childhood neoplasms is
                      usually explained by a maturation block originating in the
                      prenatal phase. In contrast, reactivation of fetal genes in
                      adult malignancies is considered a consequence of oncofetal
                      reprogramming (OFR) and is associated with aggressive
                      disease. By reconstructing epigenetic ontogeny in juvenile
                      myelomonocytic leukemia (JMML), we identified a postnatal
                      maturation state of JMML stem cells with high
                      transcriptional plasticity indicative of OFR in high-risk
                      disease. Similarly, post-natal activation of oncogenic
                      signaling by inducible Ptpn11E76K mutation in mice,
                      triggered molecular plasticity and reactivation of fetal
                      gene expression. Integrative multi-omics analysis revealed
                      aberrant CD52 expression as a feature of high-risk JMML stem
                      cells. Anti-CD52 treatment depleted JMML stem cells and
                      blocked disease propagation in xenograft models. Our results
                      challenge the prevailing maturation-block model of pediatric
                      leukemogenesis and establish RAS-associated stem-cell
                      plasticity as a determinant of OFR and potential therapeutic
                      vulnerabilities in high-risk JMML.},
      subtyp        = {Review Article},
      cin          = {B340 / W192 / A010 / A012 / W610 / B260 / HD01 / FR01 /
                      B370},
      ddc          = {610},
      cid          = {I:(DE-He78)B340-20160331 / I:(DE-He78)W192-20160331 /
                      I:(DE-He78)A010-20160331 / I:(DE-He78)A012-20160331 /
                      I:(DE-He78)W610-20160331 / I:(DE-He78)B260-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)FR01-20160331 /
                      I:(DE-He78)B370-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41348944},
      doi          = {10.1158/2643-3230.BCD-25-0246},
      url          = {https://inrepo02.dkfz.de/record/306830},
}