ReviewFrontiers in immunology2016
Role of Redox Status in Development of Glioblastoma.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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
88 citing papers in PubMed, 139 citations in OpenAlex.
- A Selective Pro-Oxidant Drives Redox Reprogramming to Induce Ferroptosis and Immune Remodeling in Glioblastoma.Smart medicine · 2026Article
- Redox Regulation in Glioblastoma: Mechanisms, Biomarkers, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Selective Cytotoxic and Redox-Associated Effects of Plant-Derived Terpenoids in Human Glioblastoma Cells.Cell biochemistry and biophysics · 2026Article
- Aromatic amino acid metabolism shapes autophagy-mediated adaptation to iron deprivation in glioblastoma cells.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Redox rewiring in glioblastoma: the thioredoxin system as a precision therapeutic target.Pharmacological reports : PR · 2026Review
- Review
- Heterogeneity, Measurement, and Clinical Implications of Oxygenation, Cell Signaling, and Redox Biology in Glioblastoma and Adult Diffuse Gliomas, with Context from Other Brain Tumors.Antioxidants (Basel, Switzerland) · 2026Review
- In vivo characterization of the redox balance in IDH-wildtype glioblastomas: a J-difference edited MEGA-sLASER MRS study at 3T.Cancer & metabolism · 2026Article
- Single-Cell Analysis Delineates Glutathione Metabolism-Related Gene Signatures in the Glioblastoma Microenvironment and Identifies GSTA4 as a Regulator of Malignant Behaviors.International journal of genomics · 2026Article
- A Comprehensive Analysis of Natural Bioactive Molecules for the Treatment and Control of Glioblastoma Multiforme (GBM) Targeting Underlying Molecular Mechanism.Chemistry & biodiversity · 2026Review
- Novel Adamantane-Sclareol Hybrids Exploit ROS Vulnerability to Overcome Multidrug-Resistance in Glioblastoma Cells.Molecules (Basel, Switzerland) · 2025Article
- Manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) represses sulfide:quinone oxidoreductase expression and targets the sulfido-redox system in glioblastoma models.Redox report : communications in free radical research · 2025Article
- Small molecular weight polyfluoroalkyl phosphonates induce ROS-mediated cytotoxicity in glioblastoma cells: a molecular mechanism study.Scientific reports · 2025Article
- Troxerutin Potentiated Temozolomide Induced Antitumor Effect in 2D and 3D Glioblastoma Models.Journal of cellular and molecular medicine · 2025Article
- Correlation between serum GFAP and 3-NT levels and the degree of neuronal injury in patients with glioma after surgery, and its diagnostic value.Biomarkers in medicine · 2025Article
- Redox-Regulated Pathways in Glioblastoma Stem-like Cells: Mechanistic Insights and Therapeutic Implications.Brain sciences · 2025Review
- Environmental Hazards and Glial Brain Tumors: Association or Causation?International journal of molecular sciences · 2025Review
- Polymeric Nanoparticle-Mediated Photodynamic Therapy: A Synergistic Approach for Glioblastoma Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Latent Association Between Diets and Glioma Risk: A Mendelian Randomization Analysis.Nutrients · 2025Article
- LB-100 Enhances Drugs Efficacy Through Inhibition of P-Glycoprotein Expression in Multidrug-Resistant Glioblastoma and Non-Small Cell Lung Carcinoma Cellular Models.Pharmaceutics · 2025Article
28 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is a highly aggressive neoplasia, prognosis remains dismal, and current therapy is mostly palliative. There are no known risk factors associated with gliomagenesis; however, it is well established that chronic inflammation in brain tissue induces oxidative stress in astrocytes and microglia. High quantities of reactive species of oxygen into the cells can react with several macromolecules, including chromosomal and mitochondrial DNA, leading to damage and malfunction of DNA repair enzymes. These changes bring genetic instability and abnormal metabolic processes, favoring oxidative environment and increase rate of cell proliferation. In GBM, a high metabolic rate and increased basal levels of reactive oxygen species play an important role as chemical mediators in the regulation of signal transduction, protecting malignant cells from apoptosis, thus creating an immunosuppressive environment. New redox therapeutics could reduce oxidative stress preventing cellular damage and high mutation rate accompanied by chromosomal instability, reducing the immunosuppressive environment. In addition, therapies directed to modulate redox rate reduce resistance and moderate the high rate of cell proliferation, favoring apoptosis of tumoral cells. This review describes the redox status in GBM, and how this imbalance could promote gliomagenesis through genomic and mitochondrial DNA damage, inducing the pro-oxidant and proinflammatory environment involved in tumor cell proliferation, resistance, and immune escape. In addition, some therapeutic agents that modulate redox status and might be advantageous in therapy against GBM are described.
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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.