ReviewDiscover oncology2024
The two-sided battlefield of tumour-associated macrophages in glioblastoma: unravelling their therapeutic potential.
Review in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- cRGD-Functionalized macrophage extracellular vesicles loaded with GSK2033 enhance T cell antitumor immunity in GBM by disrupting the LXR/ABCA1-Mediated Myelin lipid transfer axis.Journal of nanobiotechnology · 2026Article
- Network-driven prioritization and functional phenotyping nominate TTC23 as a biomarker-informed target in chlorpromazine repurposing for glioblastoma.Frontiers in pharmacology · 2026Article
- M2 macrophage infiltration associated with CXCL8 predicts grade 4 prognosis and differentiates glioma grades.Discover oncology · 2025Article
- Global research trends on Chinese patent drugs inducing programmed cell death in cancer: a bibliometric analysis (1998-2024).Discover oncology · 2025Article
- Identification of CWH43 as a novel prognostic biomarker and therapeutic target in clear cell renal cell carcinoma by a multi-omics approach and correlation with autophagy progression.Discover oncology · 2025Article
- Unraveling the significance of cuproptosis in hepatocellular carcinoma heterogeneity and tumor microenvironment through integrated single-cell sequencing and machine learning approaches.Discover oncology · 2025Article
- ATP6AP1 drives pyroptosis-mediated immune evasion in hepatocellular carcinoma: a machine learning-guided therapeutic target.Discover oncology · 2025Article
- Development of a machine learning-derived programmed cell death index for prognostic prediction and immune insights in colorectal cancer.Discover oncology · 2025Article
- Exploring novel biomarkers and immunotherapeutic targets for biofeedback therapies to reveal the tumor-associated immune microenvironment through a multimetric analysis of kidney renal clear cell carcinoma.Discover oncology · 2025Article
- Joint exposure to PMFrontiers in public health · 2025Article
- Integrating multi-omics and experimental techniques to decode ubiquitinated protein modifications in hepatocellular carcinoma.Frontiers in pharmacology · 2025Article
- Trigeminal nerve-driven neurogenic inflammation linking migraine to glioblastoma invasion: a literature review.Frontiers in immunology · 2025Review
- Clinical decision-making for uveal melanoma radiotherapy: comparative performance of experienced radiation oncologists and leading generative AI models.Frontiers in oncology · 2025Article
- Targeting the neuroimmune axis in glioblastoma: emerging strategies for precision immunotherapy.Frontiers in immunology · 2025Review
- The role of immune- and lipid metabolism-related genes in macrophage polarization and prognosis of glioblastoma.Frontiers in oncology · 2025Article
- From innate-like to innate: the next wave of off-the-shelf CAR immunotherapies.Frontiers in immunology · 2025Review
- Article
- Exploring the role of Disulfidptosis in glioma progression: insights into tumor heterogeneity and therapeutic potential through single-cell RNA sequencing.Discover oncology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Gliomas are the most common primary malignant tumours of the central nervous system (CNS), which are highly aggressive, with increasing morbidity and mortality rates year after year, posing a serious threat to the quality and expected survival time of patients. The treatment of gliomas is a major challenge in the field of neuro-oncology, especially high-grade gliomas such as glioblastomas (GBMs). Despite considerable progress in recent years in the study of the molecular and cellular mechanisms of GBMs, their prognosis remains bleak. Tumour-associated macrophages (TAMs) account for up to 50% of GBMs, and they are a highly heterogeneous cell population whose role cannot be ignored. Here, we focus on reviewing the contribution of classically activated M1-phenotype TAMs and alternatively activated M2-phenotype TAMs to GBMs, and exploring the research progress in reprogramming M1 TAMs into M2 TAMs.
Indexed as
Identifiers
What 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.