ReviewInternational journal of molecular sciences2016
ROS and Brain Gliomas: An Overview of Potential and Innovative Therapeutic Strategies.
Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed.
- 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
- Propofol and Glioblastoma Biology: A Narrative Review of Perioperative Clinical Evidence and PI3K/AKT-Wnt-miRNA, GABA-A, and Immune-Checkpoint Pathways.BioMed research international · 2026Review
- Oxidative Stress and Iron Addiction: A Comparative Study of 1321N1 Astrocytoma and T98G Glioblastoma Cells with Differential Expression of L-Cysteine-Metabolizing Enzymes.Biomolecules · 2025Article
- Troxerutin Potentiated Temozolomide Induced Antitumor Effect in 2D and 3D Glioblastoma Models.Journal of cellular and molecular medicine · 2025Article
- Targeting the Mitochondria in High-Grade Gliomas.Cancers · 2025Review
- Exploring the effects of ROS on PI3K/AKT/mTOR signalling in pediatric low-grade glioma and therapeutic strategies.Molecular biology reports · 2025Review
- Environmental Hazards and Glial Brain Tumors: Association or Causation?International journal of molecular sciences · 2025Review
- MitCOM-based prognostic model identifies GLUD1 as a key suppressor of glioblastoma growth and invasion through regulation of mitochondrial structure and metabolism.Cancer cell international · 2025Article
- The Role of Viruses in the Glioma Tumor Microenvironment: Immunosuppressors or Primers for Anti-Tumor Immunity?Cancers · 2025Review
- Non-immune targeting of CXCR3 compromises mitochondrial function and suppresses tumor growth in glioblastoma.Cell death discovery · 2025Article
- Potential of Curcumin and Its Analogs in Glioblastoma Therapy.Antioxidants (Basel, Switzerland) · 2025Review
- Unlocking the therapeutic potential of tumor-derived EVs in ischemia-reperfusion: a breakthrough perspective from glioma and stroke.Journal of neuroinflammation · 2025Review
- Latent Association Between Diets and Glioma Risk: A Mendelian Randomization Analysis.Nutrients · 2025Article
- Identification of a Novel Oxidative Stress-Based Molecular Classification and Treatment Vulnerabilities in WHO Grade 2/3 Meningiomas.Oncology research · 2025Article
- Pilot Screening of TREM1 Inhibitors in Cell-Based Reporter Assays Reflecting TREM1/DAP12 Receptor Assembly and Functionality.ACS chemical neuroscience · 2025Article
- Essential Oils from Citrus Peels Promote Calcium Overload-Induced Calcicoptosis in U251 Cells.Antioxidants (Basel, Switzerland) · 2024Article
- The Role and Applied Value of Mitochondria in Glioma-Related Research.CNS neuroscience & therapeutics · 2024Review
- A reactive oxygen species-related signature predicts the prognosis and immunosuppressive microenvironment in gliomas.Redox report : communications in free radical research · 2024Article
- Article
- Viral-Porphyrin Combo: Photodynamic and Oncolytic Viral Therapy for Potent Glioblastoma Treatment.International journal of molecular sciences · 2024Article
7 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) represent reactive products belonging to the partial reduction of oxygen. It has been reported that ROS are involved in different signaling pathways to control cellular stability. Under normal conditions, the correct function of redox systems leads to the prevention of cell oxidative damage. When ROS exceed the antioxidant defense system, cellular stress occurs. The cellular redox impairment is strictly related to tumorigenesis. Tumor cells, through the generation of hydrogen peroxide, tend to the alteration of cell cycle phases and, finally to cancer progression. In adults, the most common form of primary malignant brain tumors is represented by gliomas. The gliomagenesis is characterized by numerous molecular processes all characterized by an altered production of growth factor receptors. The difficulty to treat brain cancer depends on several biological mechanisms such as failure of drug delivery through the blood-brain barrier, tumor response to chemotherapy, and intrinsic resistance of tumor cells. Understanding the mechanisms of ROS action could allow the formulation of new therapeutic protocols to treat brain gliomas.
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