ReviewNeuro-oncology advances
Targeting immune microenvironment-mediated mesenchymal transition in glioblastoma: Molecular mechanisms and translational strategies.
Review in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma remains uniformly lethal due to profound phenotypic plasticity and adaptive resistance. The proneural-to-mesenchymal transition (PMT) has emerged as a central axis functionally linking immune evasion, metabolic rewiring, and lineage remodeling. Relevant studies tend to interrogate the tumor microenvironment in a cell-type-specific manner, whereas accumulating evidence shows that PMT is not imposed by single populations but results from coordinated inputs of macrophages, T cells, neutrophils, astrocytes, and stromal partners through polarization dynamics, cytokine circuits (IL-6, TGF-β, IL-10), and metabolic modules (eg the lactate-HIF1a axis). Therapeutic strategies that distort this PMT-permissive ecosystem, including macrophage reprogramming (GM-CSF, CSF-1R blockade), immune checkpoint inhibition, metabolic targeting, and epigenetic modulation, have shown preliminary signals yet are constrained by redundancy, spatial heterogeneity, and compensatory feedback. This review reframes the immune microenvironment as a multicellular PMT-enforcing network, synthesizes cross-cell-type mechanistic evidence, and appraises translational attempts through the lens of PMT enforcement, while outlining opportunities such as biomarker-aligned stratification, spatial multi-omics guidance, and rational combinations designed to intercept PMT circuits. Anchoring therapeutic innovation in immune-driven PMT may provide a tractable entry to overcome resistance in glioblastoma.
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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.