ReviewFrontiers in oncology2026
Targeting NOTCH-immune crosstalk in gliomas: from mechanisms to therapeutics.
Review in Frontiers in oncology, 2026. 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
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Glioblastoma (GBM) is a highly aggressive and treatment-resistant malignancy characterized by an immunosuppressive tumor microenvironment (TME) that promotes disease progression and poor clinical outcomes. Increasing evidence suggests that NOTCH signaling is a key regulator of GBM progression, governing both tumor cell plasticity and immune evasion. In addition to its roles in development and stem cell maintenance, NOTCH signaling modulates interactions among glioma stem-like cells, immune cells, and stromal components. NOTCH signaling in both tumor and stromal compartments modulates immune cell fate decisions, antigen presentation, and inflammatory cytokine expression. This suggests its potential role as a key modulator of immune crosstalk within the TME of GBM. Moreover, dysregulation of the NOTCH signaling pathway may lead to an immunosuppressive TME, enhance tumor heterogeneity, and restrict responses to conventional therapies. Recent investigations also reveal the epigenetic and non-coding RNA patterns that reinforce aberrant NOTCH activity in GBM. Understanding the multifaceted interactions among NOTCH signaling, oncogenic pathways, and immunomodulatory mechanisms could provide insights into the molecular pathogenesis of GBM progression. Here, we discuss the pleiotropic and context-dependent functions of NOTCH signaling in GBM, with particular emphasis on its implications for tumor-immune interactions and its potential as a therapeutic target to address immune escape and treatment resistance.
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.