ArticleScience advances2025
Glioblastoma exploits ATP from leading-edge astrocytes to fuel its infiltrative growth revealed by spatially resolved chimeric analysis.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Engineering an AIEgen-based platform integrating CRISPR/Cas9 to remodel the tumor microenvironment and reinforce photo-immunotherapy against glioblastom.Signal transduction and targeted therapy · 2026Article
- Astrocyte-driven immunosuppression in the brain tumor microenvironment.Nature immunology · 2026Review
- Local Tumor Microenvironment Niches Correlate With Survival And Immunotherapy Response In Human Glioblastoma.bioRxiv : the preprint server for biology · 2026Article
- Decoding myeloid heterogeneity in glioblastoma: spatial insights from transcriptomics.Journal of translational medicine · 2026Review
- Reconstructing the glioblastoma microenvironment in heterotypic 3D spheroids: a multicellular model to study tumor-stromal crosstalk.Frontiers in bioengineering and biotechnology · 2026Article
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
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Authors and funding
14 authors.
Funding
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Abstract
Glioblastoma (GBM) is the deadliest primary brain tumor that frequently infiltrates surrounding brain tissue, causing therapy resistance and recurrence. The molecular characteristics of infiltrating GBM cells and their interactions with brain cells remain poorly understood, partly due to limited spatial tools for distinguishing tumor cells from those in the tumor microenvironment (TME). Here, we introduce Spatially-resolved Chimeric AnalyzeR (SCAR), a computational tool for dissecting tumor-TME gene expression in spatial transcriptomics of human-mouse chimeric cancer models. SCAR reveals spatially distinct characteristics of GBM and their interactions with TME, identifying that infiltrative GBM up-regulates creatine kinase brain type (CKB) at the astrocyte-enriched leading edge compared to the tumor core. Mechanistically, GBM-secreted CKB catalyzes the extracellular conversion of astrocyte-supplied adenosine triphosphate (ATP) and creatine into phosphocreatine, providing metabolic support for infiltrative tumor growth, which can be blocked by cyclocreatine. These results provide proof-of-concept validation of SCAR and demonstrate spatial context-dependent metabolic rewiring of GBM cells, with implications for therapies targeting infiltrative GBM.
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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 Socratic graph.