ReviewExperimental & molecular medicine2020
ROS in cancer therapy: the bright side of the moon.
Review in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,010 papers, 1 of them a synthesis that pooled it.
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
1,010 citing papers in PubMed, 1 synthesis or guideline pooled it, 2,087 citations in OpenAlex.
- Linking Hyperuricemia to Cancer: Emerging Evidence on Risk and Progression.Current oncology reports · 2025Pooled it
- Chemical vs Physical Radioenhancement from TiONano letters · 2025Trial
- Theranostic Potential of an NAD(P)H-Activatable Fluorophore: Assessing Cancer Aggressiveness and Triggering Apoptosis.Angewandte Chemie (International ed. in English) · 2026Article
- Article
- Galloyl-RGD induces oxidative stress-mediated apoptosis in human melanoma cells.Molecular and cellular biochemistry · 2026Article
- Boric Acid Combined with Venetoclax Induces Apoptosis in CLL Cell Lines via Caspase Activation and Oxidative Stress Modulation: In Vitro and In Silico Study.Biological trace element research · 2026Article
- Article
- Redox Regulation in Glioblastoma: Mechanisms, Biomarkers, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Targeting Reactive Species Stress and Nutrient Sensing to Enhance NK-Cell Function: Mechanistic Strategies for Overcoming Pancreatic Cancer Progression and Resistance Through Supplement Therapy.International journal of molecular sciences · 2026Review
- Cancer-related pain: A bidirectional modulator of cancer progression.Clinical and translational medicine · 2026Review
- TRAF4 promotes nasopharyngeal carcinoma progression by stabilizing SETDB1 to suppress mitochondrial apoptosis.Molecular and cellular biochemistry · 2026Article
- Glutathione reductase deficiency potentiates the immunogenicity of ferroptosis and cuproptosis via amplified reactive oxygen species accumulation and cGAS-STING pathway activation.Journal of hematology & oncology · 2026Article
- Cytotoxic Potential of Marine-Derived Fungi Isolated from Sponges and Brown Algae of Mauritius.Marine drugs · 2026Article
- Updates on the Strategies to Improve the Anti-Tumor Efficacy of Ferulic Acid.International journal of molecular sciences · 2026Review
- Catalase Defines Radiotherapy Resistance and a Therapeutic Vulnerability in Rhabdomyosarcoma.International journal of molecular sciences · 2026Article
- Lipid peroxidation in cancer: a double-edged sword shaping progression and therapy.Medical oncology (Northwood, London, England) · 2026Review
- Adaptation of the Transcriptome and miRNAome in Response to Hepatocellular Hypoxia.International journal of molecular sciences · 2026Article
- On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026Review
- Intratumoral Hypoxia Triggers Mitochondrial BHLHE40 ROS Sensing Pathway to Promote Radioresistance in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Redox-regulated cell death in gastric cancer: Molecular insights and therapeutic opportunities.Journal of physiology and biochemistry · 2026Review
950 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
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) constitute a group of highly reactive molecules that have evolved as regulators of important signaling pathways. It is now well accepted that moderate levels of ROS are required for several cellular functions, including gene expression. The production of ROS is elevated in tumor cells as a consequence of increased metabolic rate, gene mutation and relative hypoxia, and excess ROS are quenched by increased antioxidant enzymatic and nonenzymatic pathways in the same cells. Moderate increases of ROS contribute to several pathologic conditions, among which are tumor promotion and progression, as they are involved in different signaling pathways and induce DNA mutation. However, ROS are also able to trigger programmed cell death (PCD). Our review will emphasize the molecular mechanisms useful for the development of therapeutic strategies that are based on modulating ROS levels to treat cancer. Specifically, we will report on the growing data that highlight the role of ROS generated by different metabolic pathways as Trojan horses to eliminate cancer cells.
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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.