% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Bessler:307548,
      author       = {N. Bessler and A. K. L. Wezenaar and H. C. R. Ariese and C.
                      Honhoff and N. Dommann and E. J. Wehrens and C. Ruiz Moreno
                      and T. J. M. van den Broek and R. V. U. Collot and D. J.
                      Kloosterman and F. Keramati and M. Roosen and S. de Blank
                      and E. van Vliet and M. Barrera Román and L. C. D. E. Gatti
                      and A. Ertürk and J. Kuball and Z. Sebestyén and M.
                      Kool$^*$ and S. Patrizi and E. Miele and A. Künkele and M.
                      E. G. Kranendonk and A. M. Cornel and S. Nierkens and C.
                      Mayer and H. G. Stunnenberg and A. Alemany and M. Alieva and
                      A. C. Rios},
      title        = {{D}e novo {H}3.3{K}27{M}-altered diffuse midline glioma in
                      human brainstem organoids to dissect {GD}2 {CAR} {T} cell
                      function.},
      journal      = {Nature cancer},
      volume       = {nn},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2026-00045},
      pages        = {nn},
      year         = {2026},
      note         = {#DKTKZFB26# / epub},
      abstract     = {Diffuse midline glioma (DMG) is a highly aggressive and
                      untreatable pediatric cancer primarily arising in the
                      pontine brainstem region, necessitating the development of
                      representative models for treatment advance. Here we
                      developed an FGF4-driven human brainstem organoid model,
                      which we used to genetically engineer H3.3K27M-altered DMG.
                      We demonstrated that brainstem pontine glial specification
                      is critical for DMG tumorigenesis, yielding infiltrative
                      tumors that recapitulate patient-representative intratumoral
                      heterogeneity. Prolonged GD2 chimeric antigen receptor (CAR)
                      T cell treatment mirrored clinical outcomes and revealed
                      extensive transcriptional heterogeneity, from which both
                      potent effector and dysfunctional CAR T cell populations
                      could be identified. Furthermore, incorporation of myeloid
                      cells generated DMG-specific microglia that reduced
                      treatment efficacy and revealed CAR T cell functional states
                      most vulnerable to microglia-mediated immunosuppression.
                      Thus, we present a representative DMG model offering a
                      months-long experimental window in vitro, which we leveraged
                      to delineate CAR T cell functionality and microglial impact,
                      aiding therapy development for this devastating disease.},
      cin          = {B062 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41492091},
      doi          = {10.1038/s43018-025-01084-0},
      url          = {https://inrepo02.dkfz.de/record/307548},
}