ArticleGlia2020
Genetic driver mutations introduced in identical cell-of-origin in murine glioblastoma reveal distinct immune landscapes but similar response to checkpoint blockade.
Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- Integrative bulk and single-cell analyses implicate ASL in MIF-associated myeloid programs in glioblastoma.Functional & integrative genomics · 2026Article
- Mismatch repair deficiency drives malignant progression and alters the tumor immune microenvironment in glioblastoma models.The Journal of clinical investigation · 2026Article
- A prognostic matrix gene expression signature defines functional glioblastoma phenotypes and niches.Communications biology · 2026Article
- Integrating biocomputational techniques for vaccine development for glioblastoma multiforme: a possible way of enhancing precision.Frontiers in immunology · 2026Review
- CDK12 regulates cellular metabolism to promote glioblastoma growth.JCI insight · 2025Article
- Single-cell dissection of the genotype-immunophenotype relationship in glioblastoma.Brain : a journal of neurology · 2025Article
- Review
- A clinically relevant model and method to study necrosis as a driving force in glioma restructuring and progression.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Microtubule actin crosslinking factor 1, a brain tumor oncoprotein (Review).Molecular and clinical oncology · 2025Review
- Markers of tumor-associated macrophages and microglia exhibit high intratumoral heterogeneity in human glioblastoma tissue.Oncoimmunology · 2024Article
- ERK signaling promotes resistance to TRK kinase inhibition in NTRK fusion-driven glioma mouse models.Cell reports · 2024Article
- Overcoming therapeutic resistance in oncolytic herpes virotherapy by targeting IGF2BP3-induced NETosis in malignant glioma.Nature communications · 2024Article
- Article
- Neutrophils in glioma microenvironment: from immune function to immunotherapy.Frontiers in immunology · 2024Review
- Roles in Innate Immunity.Advances in neurobiology · 2024Review
- A paracrine circuit of IL-1β/IL-1R1 between myeloid and tumor cells drives genotype-dependent glioblastoma progression.The Journal of clinical investigation · 2023Article
- Driver Mutations Dictate the Immunologic Landscape and Response to Checkpoint Immunotherapy of Glioblastoma.Cancer immunology research · 2023Article
- Monocyte depletion enhances neutrophil influx and proneural to mesenchymal transition in glioblastoma.Nature communications · 2023Article
- Immune checkpoint blockade in glioblastoma: from tumor heterogeneity to personalized treatment.The Journal of clinical investigation · 2023Review
- Monocyte-neutrophil entanglement in glioblastoma.The Journal of clinical investigation · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive primary brain tumor. In addition to being genetically heterogeneous, GBMs are also immunologically heterogeneous. However, whether the differences in immune microenvironment are driven by genetic driver mutation is unexplored. By leveraging the versatile RCAS/tv-a somatic gene transfer system, we establish a mouse model for Classical GBM by introducing EGFRvIII expression in Nestin-positive neural stem/progenitor cells in adult mice. Along with our previously published Nf1-silenced and PDGFB-overexpressing models, we investigate the immune microenvironments of the three models of human GBM subtypes by unbiased multiplex profiling. We demonstrate that both the quantity and composition of the microenvironmental myeloid cells are dictated by the genetic driver mutations, closely mimicking what was observed in human GBM subtypes. These myeloid cells express high levels of the immune checkpoint protein PD-L1; however, PD-L1 targeted therapies alone or in combination with irradiation are unable to increase the survival time of tumor-bearing mice regardless of the driver mutations, reflecting the outcomes of recent human trials. Together, these results highlight the critical utility of immunocompetent mouse models for preclinical studies of GBM, making these models indispensable tools for understanding the resistance mechanisms of immune checkpoint blockade in GBM and immune cell-targeting drug discovery.
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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.