ArticleProceedings of the National Academy of Sciences of the United States of America2023
Tumor progression is independent of tumor-associated macrophages in cell lineage-based mouse models of glioblastoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed.
- Ubiquitin signaling in tumor-associated macrophage reprogramming: mechanisms and therapeutic opportunities in cancers.Biomarker research · 2026Review
- Integrated 3D light sheet and 2D multiplex imaging for deep histological characterization of somatic mouse glioblastoma.iScience · 2026Article
- Consensus statement on microglial and macrophage functions in gliomas.Acta neuropathologica · 2026Review
- Decoding myeloid heterogeneity in glioblastoma: spatial insights from transcriptomics.Journal of translational medicine · 2026Review
- Interrogation of glioma immune microenvironment identifies a non-canonical role for microglial Galectin-9 in tumor cell adhesion and phagocytosis.Frontiers in immunology · 2026Article
- Role of Colony Stimulating Factor 1 (CSF-1) and Its Receptor CSF1R: Macrophage Repolarization for Glioblastoma Treatment.ACS pharmacology & translational science · 2025Review
- Single-cell dissection of the genotype-immunophenotype relationship in glioblastoma.Brain : a journal of neurology · 2025Article
- Triggering receptor expressed on myeloid cells 2 (TREM2) regulates phagocytosis in glioblastoma.Neuro-oncology · 2024Article
- The ins and outs of microglial cells in brain health and disease.Frontiers in immunology · 2024Review
- A novel disulfidptosis-related gene signature predicts overall survival of glioblastoma patients.Future science OA · 2024Article
- Tumor progression is independent of tumor-associated macrophages in cell lineage-based mouse models of glioblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Macrophage targeting therapies have had limited clinical success in glioblastoma (GBM). Further understanding the GBM immune microenvironment is critical for refining immunotherapeutic approaches. Here, we use genetically engineered mouse models and orthotopic transplantation-based GBM models with identical driver mutations and unique cells of origin to examine the role of tumor cell lineage in shaping the immune microenvironment and response to tumor-associated macrophage (TAM) depletion therapy. We show that oligodendrocyte progenitor cell lineage-associated GBMs (Type 2) recruit more immune infiltrates and specifically monocyte-derived macrophages than subventricular zone neural stem cell-associated GBMs (Type 1). We then devise a TAM depletion system that offers a uniquely robust and sustained TAM depletion. We find that extensive TAM depletion in these cell lineage-based GBM models affords no survival benefit. Despite the lack of survival benefit of TAM depletion, we show that Type 1 and Type 2 GBMs have unique molecular responses to TAM depletion. In sum, we demonstrate that GBM cell lineage influences TAM ontogeny and abundance and molecular response to TAM depletion.
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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.