ReviewActa neuropathologica communications2021
Macrophages and microglia: the cerberus of glioblastoma.
Review in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 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
161 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.
- Pooled it
- Article
- FAPExperimental & molecular medicine · 2026Article
- The Invasive Margin of Glioblastoma as a Molecular Ecosystem: Spatial Heterogeneity, Tumor-Host Interactions, and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Targeting Kinase Signaling in Glioblastoma: Structural Optimization, Blood-Brain Barrier Dynamics and Combinatorial Translational Strategies.International journal of molecular sciences · 2026Review
- Integrative bulk and single-cell analyses implicate ASL in MIF-associated myeloid programs in glioblastoma.Functional & integrative genomics · 2026Article
- Review
- Complement C5a/C5aR1 pathway facilitates glioblastoma progression via fostering glioma stem cell-macrophage symbiosis.Journal of neuroinflammation · 2026Article
- Review
- Exosomal NEAT1 from tumor stem cells induces SIRPAJournal of experimental & clinical cancer research : CR · 2026Article
- Microglia-specificity of different markers is overridden in glioblastoma specimens.Scientific reports · 2026Article
- Single-cell profiling identifies a pro-tumoral VCAN positive macrophage subset and defines a prognostic signature in glioblastoma.Discover oncology · 2026Article
- Redox rewiring in glioblastoma: the thioredoxin system as a precision therapeutic target.Pharmacological reports : PR · 2026Review
- Dual-Function Lipid-Based Nanovector Strategy for Glioblastoma Immunotherapy: STING Activation and M1 Microglia Polarization.Drug development research · 2026Review
- Tumor-associated macrophages promote ferroptosis resistance in glioblastoma by stimulating iron-loaded extracellular vesicle release.Journal of neuro-oncology · 2026Article
- Beyond Resection: Surgery as an Evolutionary Bottleneck Shaping Tumor Evolution and Treatment Response in Diffuse Gliomas.Cancers · 2026Review
- Article
- Article
- Host TLR4 activation by tenascin-C is associated with MMP14-dependent glioma invasion.Frontiers in oncology · 2026Article
- Engineered nanomedicine remodels the postoperative cavity microenvironment to suppress glioblastoma recurrence.Theranostics · 2026Review
101 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive and deadliest of the primary brain tumors, characterized by malignant growth, invasion into the brain parenchyma, and resistance to therapy. GBM is a heterogeneous disease characterized by high degrees of both inter- and intra-tumor heterogeneity. Another layer of complexity arises from the unique brain microenvironment in which GBM develops and grows. The GBM microenvironment consists of neoplastic and non-neoplastic cells. The most abundant non-neoplastic cells are those of the innate immune system, called tumor-associated macrophages (TAMs). TAMs constitute up to 40% of the tumor mass and consist of both brain-resident microglia and bone marrow-derived myeloid cells from the periphery. Although genetically stable, TAMs can change their expression profiles based upon the signals that they receive from tumor cells; therefore, heterogeneity in GBM creates heterogeneity in TAMs. By interacting with tumor cells and with the other non-neoplastic cells in the tumor microenvironment, TAMs promote tumor progression. Here, we review the origin, heterogeneity, and functional roles of TAMs. In addition, we discuss the prospects of therapeutically targeting TAMs alone or in combination with standard or newly-emerging GBM targeting therapies.
Indexed as
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.