ReviewCancer gene therapy2025
Glioblastoma-associated macrophages in glioblastoma: from their function and mechanism to therapeutic advances.
Review in Cancer gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- RNA Expression Signatures in Glioblastoma: A Systematic Review of Tumour Biology and Therapeutic Targets.Oncology research · 2025Pooled it
- The M1/M2 Test System for Determining Macrophage Phenotypes.International journal of molecular sciences · 2026Review
- Organoids to Model Tumor Microenvironment in Progression of Pathogenesis and Treatment Resistance in Glioblastoma Multiforme.Brain sciences · 2026Review
- Dual-Function Lipid-Based Nanovector Strategy for Glioblastoma Immunotherapy: STING Activation and M1 Microglia Polarization.Drug development research · 2026Review
- Overcoming blood-brain barrier and chemoresistance in glioblastoma by Angiopep-2-modified NK cell-derived extracellular vesicles for targeted delivery of temozolomide.Journal of nanobiotechnology · 2026Article
- Review
- Doxorubicin promotes the production of inflammatory cytokines in tumor-associated macrophages through activating lactate dehydrogenase A.Cell death discovery · 2026Article
- The Extracellular Matrix, the Silent 'Architect' of Glioma.Biomedicines · 2026Review
- Macrophage-based therapeutic strategies in glioblastoma: advancements in drug delivery and immunotherapy.Frontiers in oncology · 2026Review
- Glioblastoma Immunotherapy Adjuvants for Glial Cell Polarization Regulation.Experimental neurobiology · 2025Review
- CMTM6 drives glioblastoma progression by promoting M2 polarization and suppressing antigen presentation in microglia/macrophages.European journal of medical research · 2025Article
- Therapeutic potential of targeting macrophages and microglia in glioblastoma.Trends in pharmacological sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor in adults and has high mortality rates worldwide. GBM progression, treatment, and prognosis are influenced by the tumor microenvironment (TME), which includes immune, stromal, and tumor cells. Among them, glioblastoma-associated macrophages (GAMs) act as key regulators of GBM pathobiology. GAMs exhibit remarkable plasticity, as they can exhibit both protumor and antitumor effects. However, their function is determined by polarization and the TME. In this review, we provide a comprehensive overview of the current understanding of the biology of GAMs in GBM, including their origins, phenotypic diversity, and functional roles. We discuss the intricate crosstalk between GAMs and tumor cells, as well as other immune and stromal components, and highlight the mechanisms underlying GAM-mediated tumor progression, invasion, angiogenesis, and immune system evasion. Furthermore, we explore the therapeutic implications of targeting GAMs in GBM and discuss emerging strategies aimed at reprogramming GAMs toward an antitumorigenic phenotype or selectively depleting protumorigenic subsets. The final aim is to develop innovative therapeutic approaches that disrupt GBMs. By leveraging our increased understanding of GAM biology, we lay the foundation for transformative advances in GBM treatment to improve patient prognosis.
Indexed as
Identifiers
40307579What Socratic holds
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.