ArticleJournal of oncology2013
Tumor-associated macrophages in glioma: friend or foe?
Article in Journal of oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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
98 citing papers in PubMed.
- Akt and mTORC1 signaling as predictive biomarkers for the EGFR antibody nimotuzumab in glioblastoma.Acta neuropathologica communications · 2018Trial
- Tumor Microenvironmental Regulation of CAR T-Cell Therapy in High Risk Medulloblastoma.Research square · 2026Article
- [ACS omega · 2026Article
- Glioma‑associated microglia and macrophages as a potential target for mTOR inhibition in glioblastoma.Molecular medicine reports · 2025Article
- Innate Immune Signaling in Gliomas: Regulatory Mechanisms and Targeting Potential in Tumor Progression.Life (Basel, Switzerland) · 2025Review
- Delineation of signaling routes that underlie differences in macrophage phenotypic states.NAR molecular medicine · 2025Article
- Review
- Dynamic monocyte changes as prognostic indicators in operable gastric cancer: a retrospective cohort analysis.Frontiers in oncology · 2025Article
- A syngeneic spontaneous zebrafish model ofeLife · 2024Article
- Current approaches in glioblastoma multiforme immunotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- Hyperbaric Oxygen Therapy as a Novel Approach to Modulating Macrophage Polarization for the Treatment of Glioblastoma.Biomedicines · 2024Article
- Review
- Immune Escape in Glioblastoma: Mechanisms of Action and Implications for Immune Checkpoint Inhibitors and CAR T-Cell Therapy.Biology · 2023Review
- Salsalate: a pleotropic anti-inflammatory drug in the treatment of diabetes, obesity, and metabolic diseases.Inflammopharmacology · 2023Review
- Radiomics for characterization of the glioma immune microenvironment.NPJ precision oncology · 2023Review
- Interaction of glioma-associated microglia/macrophages and anti-PD1 immunotherapy.Cancer immunology, immunotherapy : CII · 2023Article
- Targeting Glioblastoma-Associated Macrophages for Photodynamic Therapy Using AGuIXPharmaceutics · 2023Article
- Quinolinate promotes macrophage-induced immune tolerance in glioblastoma through the NMDAR/PPARγ signaling axis.Nature communications · 2023Article
- Impact of epigenetic reprogramming on antitumor immune responses in glioma.The Journal of clinical investigation · 2023Review
- Immunosuppressive cells in oncolytic virotherapy for glioma: challenges and solutions.Frontiers in cellular and infection microbiology · 2023Review
38 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
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophages (TAMs) contribute substantially to the tumor mass of gliomas and have been shown to play a major role in the creation of a tumor microenvironment that promotes tumor progression. Shortcomings of attempts at antiglioma immunotherapy may result from a failure to adequately address these effects. Emerging evidence supports an independent categorization of glioma TAMs as alternatively activated M2-type macrophages, in contrast to classically activated proinflammatory M1-type macrophages. These M2-type macrophages exert glioma-supportive effects through reduced anti-tumor functions, increased expression of immunosuppressive mediators, and nonimmune tumor promotion through expression of trophic and invasion-facilitating substances. Much of our work has demonstrated these features of glioma TAMs, and together with the supporting literature will be reviewed here. Additionally, the dynamics of glioma cell-TAM interaction over the course of tumor development remain poorly understood; our efforts to elucidate glioma cell-TAM dynamics are summarized. Finally, the molecular pathways which underlie M2-type TAM polarization and gene expression similarly require further investigation, and may present the most potent targets for immunotherapeutic intervention. Highlighting recent evidence implicating the transcription factor STAT3 in immunosuppressive tumorigenic glioma TAMs, we advocate for gene array-based approaches to identify yet unappreciated expression regulators and effector molecules important to M2-type glioma TAMs polarization and function within the glioma tumor microenvironment.
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.