ArticleNeuro-oncology2023
Novel murine glioblastoma models that reflect the immunotherapy resistance profile of a human disease.
Article in Neuro-oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Glioma-intrinsic MAPK/ERK signaling promotes immunotherapy efficacy through T cell infiltration and interferon responses.Nature communications · 2026Article
- Microglial fructose metabolism is essential for glioblastoma growth.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dual phagocytosis-checkpoint blockade revitalizes immune surveillance in mouse models of glioblastoma.Nature communications · 2026Article
- STING-induced blood-brain barrier opening combined with radiotherapy potentiates antitumor response in a high-grade glioma model.The Journal of clinical investigation · 2026Article
- cGAS-agonistic spherical nucleic acids reprogram the glioblastoma immune microenvironment and promote antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Current strategies and novel immunotherapeutic approaches for overcoming immune resistance in glioblastoma.Discover oncology · 2025Review
- NLRP3 Inflammasome Activation Expands the Immunosuppressive Myeloid Stroma and Antagonizes the Therapeutic Benefit of STING Activation in Glioblastoma.Cancer research communications · 2025Article
- Is modulation of immune checkpoints on glioblastoma-infiltrating myeloid cells a viable therapeutic strategy?Neuro-oncology · 2025Review
- Fc-enhanced anti-CTLA-4, anti-PD-1, doxorubicin, and ultrasound-mediated blood-brain barrier opening: A novel combinatorial immunotherapy regimen for gliomas.Neuro-oncology · 2024Article
- In vivo mouse models for adult brain tumors: Exploring tumorigenesis and advancing immunotherapy development.Neuro-oncology · 2024Review
- MAPK/ERK signaling in gliomas modulates interferon responses, T cell recruitment, microglia phenotype, and immune checkpoint blockade efficacy.bioRxiv : the preprint server for biology · 2024Article
- STING agonist 8803 reprograms the immune microenvironment and increases survival in preclinical models of glioblastoma.The Journal of clinical investigation · 2024Article
- Kunitz-type protease inhibitor TFPI2 remodels stemness and immunosuppressive tumor microenvironment in glioblastoma.Nature immunology · 2023Article
- IGF2 supports glioblastoma growth and immune evasion through a combination of tumor cell-intrinsic and -extrinsic mechanisms.Neuro-oncology advancesArticle
- Immunocompetent murine glioblastoma stem-like cell models exhibiting distinct phenotypes.Neuro-oncology advancesArticle
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe lack of murine glioblastoma models that mimic the immunobiology of human disease has impeded basic and translational immunology research. We, therefore, developed murine glioblastoma stem cell lines derived from Nestin-CreERT2QkL/L; Trp53L/L; PtenL/L (QPP) mice driven by clinically relevant genetic mutations common in human glioblastoma. This study aims to determine the immune sensitivities of these QPP lines in immunocompetent hosts and their underlying mechanisms.
methodsThe differential responsiveness of QPP lines was assessed in the brain and flank in untreated, anti-PD-1, or anti-CTLA-4 treated mice. The impact of genomic landscape on the responsiveness of each tumor was measured through whole exome sequencing. The immune microenvironments of sensitive (QPP7) versus resistant (QPP8) lines were compared in the brain using flow cytometry. Drivers of flank sensitivity versus brain resistance were also measured for QPP8.
resultsQPP lines are syngeneic to C57BL/6J mice and demonstrate varied sensitivities to T cell immune checkpoint blockade ranging from curative responses to complete resistance. Infiltrating tumor immune analysis of QPP8 reveals improved T cell fitness and augmented effector-to-suppressor ratios when implanted subcutaneously (sensitive), which are absent on implantation in the brain (resistant). Upregulation of PD-L1 across the myeloid stroma acts to establish this state of immune privilege in the brain. In contrast, QPP7 responds to checkpoint immunotherapy even in the brain likely resulting from its elevated neoantigen burden.
conclusionsThese syngeneic QPP models of glioblastoma demonstrate clinically relevant profiles of immunotherapeutic sensitivity and potential utility for both mechanistic discovery and evaluation of immune therapies.
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