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@ARTICLE{DAzorn:305229,
      author       = {D. D Azorín$^*$ and D. C. F. Hoffmann$^*$ and N.
                      Hebach$^*$ and E. Jung$^*$ and D. Hausmann$^*$ and M.
                      Ratliff$^*$ and L. Hai$^*$ and S. Horschitz and A. Jabali
                      and M. Osswald$^*$ and M. A. Karreman$^*$ and T. Kessler$^*$
                      and S. Wendler$^*$ and C. D. Mayer$^*$ and C. Löb$^*$ and
                      P. Lehnert$^*$ and G. M. Cebulla$^*$ and D. Reibold$^*$ and
                      R. Khajuria$^*$ and P. Bordignon and A. E. Moor and T.
                      Holland-Letz$^*$ and J. Reckless and N. Ramsden and D.
                      Grainger and A. Kreshuk and P. Koch and W. Wick$^*$ and S.
                      Heuer$^*$ and F. Winkler$^*$},
      title        = {{S}creening for {T}umor {M}icrotube-{T}argeting {D}rugs
                      {I}dentifies {PKC} {M}odulators as {M}ultipotent
                      {I}nhibitors of {G}lioblastoma {P}rogression.},
      journal      = {Cancer discovery},
      volume       = {nn},
      issn         = {2159-8274},
      address      = {Philadelphia, Pa.},
      publisher    = {[Verlag nicht ermittelbar]},
      reportid     = {DKFZ-2025-02075},
      pages        = {nn},
      year         = {2025},
      note         = {#EA:B320#LA:B320# / epub},
      abstract     = {Glioblastomas are incurable primary brain tumors that
                      depend on neural-like cellular processes, tumor microtubes
                      (TMs), to invade the brain. TMs also interconnect single
                      tumor cells to a communicating multicellular network that
                      resists current therapies. Here, we developed a combined,
                      comprehensive in vitro/in vivo anti-TM drug screening
                      approach, including machine-learning-based analysis tools.
                      Two Protein Kinase C (PKC) modulators robustly inhibited TM
                      formation and pacemaker tumor cell-driven, TM-mediated
                      glioblastoma cell network communication. Since
                      TM-unconnected tumor cells exhibited increased sensitivity
                      to cytotoxic therapy, the PKC activator TPPB was combined
                      with radiotherapy, and long-term intravital 2-photon
                      microscopy paired with spatially resolved multiomics
                      revealed anti-TM and anti-tumor effects. TPPB treatment also
                      decreased the expression of tweety family member 1 (TTYH1),
                      a key driver of invasive TMs. Our study establishes a novel
                      screening pipeline for anti-TM drug development, identifies
                      a TM master regulator pathway, and supports the approach of
                      TM targeting for efficient brain tumor therapies.},
      cin          = {B320 / HD01 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)B320-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)C060-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41065276},
      doi          = {10.1158/2159-8290.CD-24-0414},
      url          = {https://inrepo02.dkfz.de/record/305229},
}