ArticleCell reports2026
Human organoid tumor transplantation identifies functional glioblastoma-microenvironment communication mediated by PTPRZ1.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Organoids to Model Tumor Microenvironment in Progression of Pathogenesis and Treatment Resistance in Glioblastoma Multiforme.Brain sciences · 2026Review
- Glutamatergic neuron-tumor synapses shape human glioblastoma cell states through radial glia plasticity.bioRxiv : the preprint server for biology · 2026Article
- Predictable clonal hierarchies from restricted progenitors provide a framework for cell type-specific therapies in glioblastoma.bioRxiv : the preprint server for biology · 2026Article
- A human tumor-immune organoid model of glioblastoma.Cell reports · 2026Article
- Modeling gliomas with organoids: reconstructing the human neural microenvironment for translational neuro-oncology.Frontiers in oncology · 2026Review
- Targeting Radiation-Induced Glioma-Initiating Cells in Patient-Derived Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- A Human Tumor-Immune Organoid Model of Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- The HOX Gene Family's Role as Prognostic and Diagnostic Biomarkers in Hematological and Solid Tumors.Cancers · 2025Review
- Glioblastoma Neurovascular Progenitor Orchestrates Tumor Cell Type Diversity.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
16 authors.
Funding
Abstract
Glioblastoma is the most aggressive and deadly form of brain cancer. Here, we leverage our human organoid tumor transplantation (HOTT) co-culture system to explore how extrinsic cues modulate glioblastoma cell types and behavior. HOTT recapitulates core features of major patient tumor cell types and key aspects of neural cell-enriched tumor microenvironment (nTME) gene programs. Our exploration of patient TME interactions preserved in HOTT highlights four receptor-ligand interactions of interest. We knock down all four of these genes in the HOTT microenvironment. We observe that knocking down nTME PTPRZ1, a receptor tyrosine phosphatase implicated in cancer cell migration, results in an increased fraction of mesenchymal cells, enrichment of epithelial-to-mesenchymal gene programs, and an elevated tumor microtube length in co-cultured primary patient tumors. This phenotype is not mediated by PTPRZ1's catalytic activity, suggesting a mechanism of tumor cell fate driven by nTME PTPRZ1, highlighting the strengths of the HOTT system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.