ReviewNPJ precision oncology2025
Exploring tumor-associated macrophages in glioblastoma: from diversity to therapy.
Review in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 of them syntheses 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
65 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- cGAS-STING agonists in preclinical glioblastoma animal models: a systematic review of tumor microenvironment modulation and survival outcomes.Journal of neuro-oncology · 2026Pooled it
- Unlocking glioblastoma: breakthroughs in molecular mechanisms and next-generation therapies.Medical oncology (Northwood, London, England) · 2025Pooled it
- RNA Expression Signatures in Glioblastoma: A Systematic Review of Tumour Biology and Therapeutic Targets.Oncology research · 2025Pooled it
- Article
- The Imbalance Between Tumor Immunosurveillance and Tumor Immune Escape in Glioblastoma.Immunology and cell biology · 2026Review
- Next-generation therapeutics for glioblastoma: Challenges and future directions.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- CXCL8 Enhances Malignancy of GBM via TNFα-NFκB Mediated Suppression of Ferroptosis.Applied biochemistry and biotechnology · 2026Article
- Unveiling CCL5: the master regulator of breast cancer progression and immune evasion.Breast cancer research : BCR · 2026Review
- Design, synthesis and anti-glioblastoma multiforme activity of N-methoxy-2-(pyrimidin-4-ylamino)benzamide derivatives as focal adhesion kinase inhibitors.Molecular diversity · 2026Article
- Combinatorial in situ cancer vaccines: unlocking broad and enhanced antitumor responses.Signal transduction and targeted therapy · 2026Review
- GM-CSF downregulates type I IFN responses in glioblastoma-associated monocytes.Experimental & molecular medicine · 2026Article
- Diphenyl Diselenide and Temozolomide: Downregulation of Inflammatory, Redox, and Tumor-Associated Pathways in Glioblastoma.Biological trace element research · 2026Article
- Glioma-Associated Microglia Augment Neuronal Hyper-Excitability in Glioma.Brain tumor research and treatment · 2026Review
- Multi-omics profiling-derived signature links cellular ecosystem to glioblastoma prognosis.iScience · 2026Article
- Review
- Plasma histone monomers as novel diagnostic markers in adult glioblastoma.The journal of liquid biopsy · 2026Article
- Pharmacological Ascorbate Restrains Epithelial-Mesenchymal Transition and Invasion in Glioblastoma Cells via Extracellular HInternational journal of molecular sciences · 2026Article
- Integrative Multi-Omics Analysis Identifies anGenes · 2026Article
- Organoids to Model Tumor Microenvironment in Progression of Pathogenesis and Treatment Resistance in Glioblastoma Multiforme.Brain sciences · 2026Review
- Microglia-specificity of different markers is overridden in glioblastoma specimens.Scientific reports · 2026Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Glioblastoma is the most aggressive and lethal cancer of the central nervous system, presenting substantial treatment challenges. The current standard treatment, which includes surgical resection followed by temozolomide and radiation, offers limited success. While immunotherapies, such as immune checkpoint inhibitors, have proven effective in other cancers, they have not demonstrated significant efficacy in GBM. Emerging research highlights the pivotal role of tumor-associated macrophages (TAMs) in supporting tumor growth, fostering treatment resistance, and shaping an immunosuppressive microenvironment. Preclinical studies show promising results for therapies targeting TAMs, suggesting potential in overcoming these barriers. TAMs consist of brain-resident microglia and bone marrow-derived macrophages, both exhibiting diverse phenotypes and functions within the tumor microenvironment. This review delves into the origin, heterogeneity, and functional roles of TAMs in GBM, underscoring their dual roles in tumor promotion and suppression. It also summarizes recent progress in TAM-targeted therapies, which may, in combination with other treatments like immunotherapy, pave the way for more effective and personalized strategies against this aggressive malignancy.
Identifiers
What OpenQuestion 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 OpenQuestion graph.