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@ARTICLE{MostufiZadehHaghighi:282723,
      author       = {G. Mostufi-Zadeh-Haghighi and P. Veratti$^*$ and K. Zodel
                      and G. Greve and M. Waterhouse and R. Zeiser and M. L.
                      Cleary and M. Lübbert$^*$ and J. Duque-Afonso},
      title        = {{F}unctional {C}haracterization of {T}ransforming {G}rowth
                      {F}actor-β {S}ignaling in {D}asatinib {R}esistance and
                      {P}re-{BCR}+ {A}cute {L}ymphoblastic {L}eukemia.},
      journal      = {Cancers},
      volume       = {15},
      number       = {17},
      issn         = {2072-6694},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2023-01849},
      pages        = {4328},
      year         = {2023},
      abstract     = {The multi-kinase inhibitor dasatinib has been implicated to
                      be effective in pre-B-cell receptor (pre-BCR)-positive acute
                      lymphoblastic leukemia (ALL) expressing the E2A-PBX1 fusion
                      oncoprotein. The TGFβ signaling pathway is involved in a
                      wide variety of cellular processes, including embryonic
                      development and cell homeostasis, and it can have dual roles
                      in cancer: suppressing tumor growth at early stages and
                      mediating tumor progression at later stages. In this study,
                      we identified the upregulation of the TGFβ signaling
                      pathway in our previously generated human
                      dasatinib-resistant pre-BCR+/E2A-PBX1+ ALL cells using
                      global transcriptomic analysis. We confirm the upregulation
                      of the TGFβ pathway member SMAD3 at the transcriptional and
                      translational levels in dasatinib-resistant
                      pre-BCR+/E2A-PBX1+ ALL cells. Hence, dasatinib blocks, at
                      least partially, TGFβ-induced SMAD3 phosphorylation in
                      several B-cell precursor (BCP) ALL cell lines as well as in
                      dasatinib-resistant pre-BCR+/E2A-PBX1+ ALL cells. Activation
                      of the TGFβ signaling pathway by TGF-β1 leads to growth
                      inhibition by cell cycle arrest at the G0/G1 stage, increase
                      in apoptosis and transcriptional changes of SMAD-targeted
                      genes, e.g. c-MYC downregulation, in pre-BCR+/E2A-PBX1+ ALL
                      cells. These results provide a better understanding about
                      the role that the TGFβ signaling pathway plays in
                      leukemogenesis of BCP-ALL as well as in secondary drug
                      resistance to dasatinib.},
      keywords     = {B-cell precursors (Other) / acute lymphoblastic leukemia
                      (Other) / dasatinib (Other) / drug resistance (Other) /
                      transforming growth factor-β signaling pathway (Other)},
      cin          = {FR01},
      ddc          = {610},
      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:37686604},
      pmc          = {pmc:PMC10486903},
      doi          = {10.3390/cancers15174328},
      url          = {https://inrepo02.dkfz.de/record/282723},
}