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@ARTICLE{Koleci:299576,
      author       = {N. Koleci and Y. Wu and N. A. Wehner and J. Rajak and V. R.
                      Mittapalli and J. Mergner and H. Xiao and J. Wang and M.
                      Wahl and S. Bohler and K. Aumann and G. Häcker and S.
                      Ramamoorthy and M. Boerries and S. Kirschnek and M.
                      Erlacher$^*$},
      title        = {{O}ncogenic and microenvironmental signals drive cell type
                      specific apoptosis resistance in juvenile myelomonocytic
                      leukemia.},
      journal      = {Cell death $\&$ disease},
      volume       = {16},
      number       = {1},
      issn         = {2041-4889},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2025-00517},
      pages        = {165},
      year         = {2025},
      abstract     = {Juvenile myelomonocytic leukemia (JMML) is caused by
                      constitutively activated RAS signaling and characterized by
                      increased proliferation and predominant myelomonocytic
                      differentiation of hematopoietic cells. Using
                      MxCre;Ptpn11D61Y/+ mice, which model human JMML, we show
                      that RAS pathway activation affects apoptosis signaling
                      through cell type-dependent regulation of BCL-2 family
                      members. Apoptosis resistance observed in monocytes and
                      granulocytes was mediated by overexpression of the
                      anti-apoptotic and down-regulation of the pro-apoptotic
                      members of the BCL-2 family. Two anti-apoptotic proteins,
                      BCL-XL and MCL-1, were directly regulated by the oncogenic
                      RAS signaling but, in addition, were influenced by
                      microenvironmental signals. While BCL-XL and BCL-2 were
                      required for the survival of monocytes, MCL-1 was essential
                      for neutrophils. Interestingly, stem and progenitor cells
                      expressing the oncogenic PTPN11 mutant showed no increased
                      apoptosis resistance. BCL-XL inhibition was the most
                      effective in killing myeloid cells in vitro but was
                      insufficient to completely resolve myeloproliferation in
                      vivo.},
      keywords     = {Leukemia, Myelomonocytic, Juvenile: genetics / Leukemia,
                      Myelomonocytic, Juvenile: metabolism / Leukemia,
                      Myelomonocytic, Juvenile: pathology / Apoptosis: genetics /
                      Animals / Mice / Humans / bcl-X Protein: metabolism / bcl-X
                      Protein: genetics / Signal Transduction / Myeloid Cell
                      Leukemia Sequence 1 Protein: metabolism / Myeloid Cell
                      Leukemia Sequence 1 Protein: genetics / Monocytes:
                      metabolism / Protein Tyrosine Phosphatase, Non-Receptor Type
                      11: metabolism / Protein Tyrosine Phosphatase, Non-Receptor
                      Type 11: genetics / Tumor Microenvironment / Granulocytes:
                      metabolism / Granulocytes: pathology / bcl-X Protein (NLM
                      Chemicals) / Myeloid Cell Leukemia Sequence 1 Protein (NLM
                      Chemicals) / Protein Tyrosine Phosphatase, Non-Receptor Type
                      11 (NLM Chemicals)},
      cin          = {FR01},
      ddc          = {570},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40057493},
      doi          = {10.1038/s41419-025-07479-2},
      url          = {https://inrepo02.dkfz.de/record/299576},
}