ReviewiScience2020
Incorporating Tumor-Associated Macrophages into Engineered Models of Glioma.
Review in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic review on poly(I:C) and poly-ICLC in glioblastoma: adjuvants coordinating the unlocking of immunotherapy.Journal of experimental & clinical cancer research : CR · 2021Pooled it
- Article
- Inflammasomes in glioblastoma.Journal of neuroinflammation · 2026Review
- Microfluidic approaches for liquid biopsy in glioblastoma: Insights into diagnostic and follow-up strategies.Bioengineering & translational medicine · 2026Review
- Long Non-coding RNA CRNDE Promotes the Development of Glioma by Inducing Polarization of M2-Type Macrophages.Molecular neurobiology · 2025Article
- Tumor-infiltrating myeloid cells; mechanisms, functional significance, and targeting in cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Immune-Infiltrated Cancer Spheroid Model with Vascular Recirculation Reveals Temporally Dependent and Tissue-Specific Macrophage Recruitment.Advanced healthcare materials · 2025Article
- Engineered oncolytic virus coated with anti-PD-1 and alendronate for ameliorating intratumoral T cell hypofunction.Experimental hematology & oncology · 2025Article
- Turning attention to tumor-host interface and focus on the peritumoral heterogeneity of glioblastoma.Nature communications · 2024Article
- Review
- A low level of tumor necrosis factor α in tumor microenvironment maintains the self-renewal of glioma stem cells by Vasorin-mediated glycolysis.Neuro-oncology · 2024Article
- Dissecting TGF-β-induced glioblastoma invasion with engineered hyaluronic acid hydrogels.APL bioengineering · 2024Article
- Review
- Pentraxin 3: A Main Driver of Inflammation and Immune System Dysfunction in the Tumor Microenvironment of Glioblastoma.Cancers · 2024Review
- Biomaterial-basedCancer pathogenesis and therapy · 2023Review
- Overexpression of RAB34 associates with tumor aggressiveness and immune infiltration in glioma.Bioscience reports · 2022Article
- Regulation of Tumor Invasion by the Physical Microenvironment: Lessons from Breast and Brain Cancer.Annual review of biomedical engineering · 2022Review
- The Diagnostic Significance of CXCL13 in M2 Tumor Immune Microenvironment of Human Astrocytoma.Pathology oncology research : POR · 2022Article
- The impact of tumor associated macrophages on tumor biology under the lens of mathematical modelling: A review.Frontiers in immunology · 2022Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Tumor progression is profoundly influenced by interactions between cancer cells and the tumor microenvironment (TME). Among the various non-neoplastic cells present, immune cells are critical players in tumor development and have thus emerged as attractive therapeutic targets. Malignant gliomas exhibit a unique immune landscape characterized by high numbers of tumor-associated macrophages (TAMs). Despite encouraging preclinical results, targeting TAMs has yielded limited clinical success as a strategy for slowing glioma progression. The slow translational progress of TAM-targeted therapies is due in part to an incomplete understanding of the factors driving TAM recruitment, differentiation, and polarization. Furthermore, the functions that TAMs adopt in gliomas remain largely unknown. Progress in addressing these gaps requires sophisticated culture platforms capable of capturing key cellular and physical TME features. This review summarizes the current understanding of TAMs in gliomas and highlights the utility of
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.