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@ARTICLE{Foerster:303402,
      author       = {L. C. Foerster$^*$ and O. Kaya$^*$ and V. Wüst and D.-P.
                      Danciu and V. Akçay$^*$ and M. Bekavac$^*$ and K. C.
                      Ziegler$^*$ and N. Stinchcombe$^*$ and A. Tang$^*$ and S.
                      Kleber$^*$ and J. Tang$^*$ and J. Brunken$^*$ and I.
                      Lois-Bermejo$^*$ and N. Gesteira-Perez$^*$ and X. Ma$^*$ and
                      A. Sadik$^*$ and P. U. Le and K. Petrecca and C. Opitz$^*$
                      and H. Liu$^*$ and C. R. Wirtz and A. Goncalves$^*$ and A.
                      Marciniak-Czochra and S. Anders and A. Martin-Villalba$^*$},
      title        = {{C}ross-species comparison reveals therapeutic
                      vulnerabilities halting glioblastoma progression.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01638},
      pages        = {7250},
      year         = {2025},
      note         = {#EA:A290#LA:A290#},
      abstract     = {The growth of a tumor is tightly linked to the distribution
                      of its cells along a continuum of activation states. Here,
                      we systematically decode the activation state architecture
                      (ASA) in a glioblastoma (GBM) patient cohort through
                      comparison to adult murine neural stem cells. Modelling of
                      these data forecasts how tumor cells organize to sustain
                      growth and identifies the rate of activation as the main
                      predictor of growth. Accordingly, patients with a higher
                      quiescence fraction exhibit improved outcomes. Further, DNA
                      methylation arrays enable ASA-related patient
                      stratification. Comparison of healthy and malignant gene
                      expression dynamics reveals dysregulation of the
                      Wnt-antagonist SFRP1 at the quiescence to activation
                      transition. SFRP1 overexpression renders GBM quiescent and
                      increases the overall survival of tumor-bearing mice.
                      Surprisingly, it does so through reprogramming the tumor's
                      stem-like methylome into an astrocyte-like one. Our findings
                      offer a framework for patient stratification with prognostic
                      value, biomarker identification, and therapeutic avenues to
                      halt GBM progression.},
      keywords     = {Glioblastoma: genetics / Glioblastoma: pathology /
                      Glioblastoma: metabolism / Humans / Animals / Mice / DNA
                      Methylation / Disease Progression / Brain Neoplasms:
                      pathology / Brain Neoplasms: genetics / Brain Neoplasms:
                      metabolism / Gene Expression Regulation, Neoplastic /
                      Membrane Proteins: metabolism / Membrane Proteins: genetics
                      / Neural Stem Cells: metabolism / Neural Stem Cells:
                      pathology / Intercellular Signaling Peptides and Proteins:
                      metabolism / Intercellular Signaling Peptides and Proteins:
                      genetics / Cell Line, Tumor / Neoplastic Stem Cells:
                      metabolism / Neoplastic Stem Cells: pathology / Female /
                      Male / Species Specificity / Prognosis / Membrane Proteins
                      (NLM Chemicals) / Intercellular Signaling Peptides and
                      Proteins (NLM Chemicals) / SFRP1 protein, human (NLM
                      Chemicals)},
      cin          = {A290 / A240 / B350 / HD01 / C220},
      ddc          = {500},
      cid          = {I:(DE-He78)A290-20160331 / I:(DE-He78)A240-20160331 /
                      I:(DE-He78)B350-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)C220-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40770193},
      doi          = {10.1038/s41467-025-62528-w},
      url          = {https://inrepo02.dkfz.de/record/303402},
}