ReviewCancer cell international2025
Resveratrol-mediated suppression of glioblastoma and glioma: targeting apoptosis, differentiation, and stem cell dynamics.
Review in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Nanoparticle-Based delivery of proteasome inhibitors for glioblastoma Therapy: Strategies to overcome Blood-Brain barrier and therapeutic resistance.Biochemical pharmacology · 2026Review
- Integrating Molecular Pathology, Tumor Microenvironment, and Novel Therapies to Overcome Resistance in Glioblastoma.Journal of molecular neuroscience : MN · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most aggressive type of primary brain tumor and is characterized by profound therapeutic resistance and poor survival outcomes. Resveratrol (RES), a dietary polyphenol found in grapes and berries, has attracted considerable interest for its pleiotropic antitumor activities. This review delineates the mechanistic landscape by which RES attenuates GBM progression, with emphasis on apoptosis induction, the promotion of differentiation, and the modulation of GBM stem-like cell (GSC) phenotypes. RES engages both intrinsic and extrinsic apoptotic programs, leading to caspase activation, programmed cell death, and diminished tumor viability. In parallel, RES promotes GBM cell differentiation, thereby constraining the proliferative capacity and invasive behavior of GBM cells. Notably, RES perturbs GSC maintenance by impairing self-renewal and tumorigenicity, processes central to therapeutic failure and recurrence. Through coordinated regulation of oncogenic and stress‒response pathways, RES reduces viability and stem-like features while enhancing the responsiveness of GBM cells to standard modalities, suggesting potential synergy within combinatorial regimens. Collectively, these data position RES as a promising adjunctive agent that mechanistically targets core hallmarks of GBM biology and may contribute to improved therapeutic outcomes when integrated into rational, multimodal treatment strategies.
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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.