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@ARTICLE{Xing:302014,
      author       = {Y. L. Xing and D. Panovska and J.-W. Park and S. Grossauer
                      and K. Koeck and B. Bui and E. Nasajpour and J. J. Nirschl
                      and Z.-P. Feng and P. Cheung and P. Habib and R. Wei and J.
                      Wang and W. Thomason and M. Monje and J. Xiu and A. Beck and
                      K. Weber$^*$ and P. N. Harter and M. Lim and K. B. Mahaney
                      and L. M. Prolo and G. A. Grant and X. Ji and K. M. Walsh
                      and J. M. Mulcahy Levy and D. Hambardzumyan and C. K.
                      Petritsch},
      title        = {{BRAF}/{MEK} inhibition induces cell state transitions
                      boosting immune checkpoint sensitivity in
                      {BRAFV}600{E}-mutant glioma.},
      journal      = {Cell reports / Medicine},
      volume       = {6},
      number       = {6},
      issn         = {2666-3791},
      address      = {Cambridge, MA},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2025-01212},
      pages        = {102183},
      year         = {2025},
      note         = {2025 Jun 17;6(6):102183},
      abstract     = {Resistance to v-raf murine sarcoma viral oncogene homolog
                      B1 (BRAF) plus mitogen-activated protein kinase kinase (MEK)
                      inhibition (BRAFi+MEKi) in BRAFV600E-mutant gliomas drives
                      rebound, progression, and high mortality, yet it remains
                      poorly understood. This study addresses the urgent need to
                      develop treatments for BRAFi+MEKi-resistant glioma using
                      preclinical mouse models and patient-derived materials.
                      BRAFi+MEKi reveals glioma plasticity by heightening cell
                      state transitions along glial differentiation trajectories,
                      giving rise to astrocyte- and immunomodulatory
                      oligodendrocyte (OL)-like states. PD-L1 upregulation in
                      OL-like cells links cell state transitions to immune
                      evasion, possibly orchestrated by Galectin-3. BRAFi+MEKi
                      induces interferon response signatures, tumor infiltration,
                      and suppression of T cells. Combining BRAFi+MEKi with immune
                      checkpoint inhibition enhances survival in a T
                      cell-dependent manner, reinvigorates T cells, and
                      outperforms individual or sequential therapies in mice.
                      Elevated PD-L1 expression in BRAF-mutant versus
                      BRAF-wild-type glioblastoma supports the rationale for PD-1
                      inhibition in patients. These findings underscore the
                      potential of targeting glioma plasticity and highlight
                      combination strategies to overcome therapy resistance in
                      BRAFV600E-mutant high-grade glioma.},
      keywords     = {BRAF V600E (Other) / BRAF and MEK inhibitor adaptation
                      (Other) / Galectin-3 (Other) / T cell modulation (Other) /
                      cell state transitions (Other) / high-grade glioma (Other) /
                      immune checkpoint inhibition (Other) / programmed
                      death-ligand 1 (Other)},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40505659},
      doi          = {10.1016/j.xcrm.2025.102183},
      url          = {https://inrepo02.dkfz.de/record/302014},
}