ReviewCancers2019
Metabolic Regulation of Redox Balance in Cancer.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 109 citations in OpenAlex.
- Oncometabolites in Cancer Metabolism: Mechanistic Insights and Biomarker Potential- A Narrative Review.Health science reports · 2026Article
- Ginsenoside Rg5 Targets PRDX1 to Disrupt Redox Homeostasis and Induce Mitochondria-Dependent Apoptosis in Human Hepatocellular Carcinoma HepG2 Cells.Molecules (Basel, Switzerland) · 2026Article
- Systemic dysregulation of essential and toxic elements and redox homeostasis in gynecologic malignancies.Frontiers in oncology · 2026Article
- Preoperative immunonutrition as a strategy for reducing oxidative stress and inflammation in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2026Article
- Variant-to-Biomarker Integration and Mechanistic Validation Identify CES1 as a Copy Number-Linked Predictor of Radiotherapy Response in Rectal Cancer.Human mutation · 2026Article
- Oxidative Stress-Driven Cellular Senescence: Mechanistic Crosstalk and Therapeutic Horizons.Antioxidants (Basel, Switzerland) · 2025Review
- Ablation of Steroidogenic Superoxide Dismutase 2 Increases Oxidative Stress and Diminishes Steroid Hormone Production.Endocrinology · 2025Article
- Molecular Imaging: Unveiling Metabolic Abnormalities in Pancreatic Cancer.International journal of molecular sciences · 2025Review
- Interaction of Manganese-Doped Copper Oxide Nano-Platelets with Cells: Biocompatibility and Anticancer Activity Assessment.Biomimetics (Basel, Switzerland) · 2025Article
- K-Means Clustering of HyperpolarisedCancers · 2025Article
- The impact of oxidative stress and the NRF2-KEAP1-ARE signaling pathway on anticancer drug resistance.Oncology research · 2025Review
- Additive Effects of Cu-ATSM and Radiation on Survival of Diffuse Intrinsic Pontine Glioma Cells.Radiation research · 2025Article
- Assessment of the Circulating PD-1 and PD-L1 Levels and P53 Expression as a Predictor of Relapse in Pediatric Patients with Wilms Tumor and Hypernephroma.Children (Basel, Switzerland) · 2024Article
- Metabolic landscape of the healthy pancreas and pancreatic tumor microenvironment.JCI insight · 2024Article
- Betulinic acid induces apoptosis of HeLa cells via ROS-dependent ER stress and autophagy in vitro and in vivo.Journal of natural medicines · 2024Article
- A dual model of normal vs isogenic Nrf2-depleted murine epithelial cells to explore oxidative stress involvement.Scientific reports · 2024Article
- Sigma1 Regulates Lipid Droplet-mediated Redox Homeostasis Required for Prostate Cancer Proliferation.Cancer research communications · 2023Article
- The regulation of amino acid metabolism in tumor cell death: from the perspective of physiological functions.Apoptosis : an international journal on programmed cell death · 2023Review
- Effect of Diet and Oxidative Stress in the Pathogenesis of Lymphoproliferative Disorders.Antioxidants (Basel, Switzerland) · 2023Review
- Nanoparticle-Based Antioxidants in Stress Signaling and Programmed Cell Death in Breast Cancer Treatment.Molecules (Basel, Switzerland) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) are chemically active free radicals produced by partial reduction of oxygen that can activate discrete signaling pathways or disrupt redox homeostasis depending on their concentration. ROS interacts with biomolecules, including DNA, and can cause mutations that can transform normal cells into cancer cells. Furthermore, certain cancer-causing mutations trigger alterations in cellular metabolism that can increase ROS production, resulting in genomic instability, additional DNA mutations, and tumor evolution. To prevent excess ROS-mediated toxicity, cancer-causing mutations concurrently activate pathways that manage this oxidative burden. Hence, an understanding of the metabolic pathways that regulate ROS levels is imperative for devising therapies that target tumor cells. In this review, we summarize the dual role of metabolism as a generator and inhibitor of ROS in cancer and discuss current strategies to target the ROS axis.
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.