ReviewCell death & disease2016
ROS homeostasis and metabolism: a dangerous liason in cancer cells.
Review in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 538 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
538 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,124 citations in OpenAlex.
- Redox-manipulating nanocarriers for anticancer drug delivery: a systematic review.Journal of nanobiotechnology · 2024Pooled it
- Thioredoxin reductase-1 facilitates cellular plasticity and stemness mediated by TGF-β1 in non-small cell lung cancer.Cancer biology & therapy · 2026Article
- Metabolic immune checkpoints (MICs) in cancer: from molecular mechanisms to challenges and opportunities in clinical translation.Signal transduction and targeted therapy · 2026Review
- 3D Bioprinted Blood-Brain-Tumor Barrier Spheroid-Based In Situ Evaluation of Anticancer Compounds Against Glioblastoma: ROS-Producing Ruthenium as a Potential Therapeutic Candidate.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glutamine Metabolism in Health and Diseases.MedComm · 2026Review
- Mitochondria-Directed Redox Phospholipid Polymers for Cancer Therapy.Cancer science · 2026Article
- Sequential HAngewandte Chemie (International ed. in English) · 2026Article
- NRF2 activation is required for chemotherapy resistance acquisition in medulloblastoma via metabolic and redox adaptation.Redox biology · 2026Article
- Exploiting Metabolic Vulnerabilities in Acute Myeloid Leukemia: Rationale and Evidence for Combining Metabolic Modulators with Conventional Chemotherapy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.Disease models & mechanisms · 2026Article
- Reactive Oxygen Species in Breast Cancer: From Redox Dysregulation to ROS-Responsive Therapeutics.Cell biochemistry and function · 2026Review
- A peroxiredoxin 1-reactive oxygen species feedback loop modulates nuclear factor kappa B activity in osteoclastogenesis.Molecular biomedicine · 2026Article
- Possible Applications of Cold Atmospheric Plasma in Otorhinolaryngology: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- Catalase Defines Radiotherapy Resistance and a Therapeutic Vulnerability in Rhabdomyosarcoma.International journal of molecular sciences · 2026Article
- Article
- Tumor cells escape from therapy-induced senescence: from molecular mechanisms to targeted intervention.Biology direct · 2026Review
- GSH-Related Enzymes GPx4, Chac1, and GSTs and Redox Regulation of Ferroptosis in Cancer.International journal of molecular sciences · 2026Review
- MUTYH Cancer-Associated Variants Within the Interdomain Connector Differentially Impact Glycosylase Activity and Cellular DNA Repair.Chembiochem : a European journal of chemical biology · 2026Article
- D-salicin induces oxidative stress-mediated ERK1/2 suppression and apoptosis in endometrial cancer cells.Oncology letters · 2026Article
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
478 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
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms that tumors engage in when faced with oxidative stress conditions that are critical for cancer progression by producing redox cofactors. In particular, we describe how the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells. Last, we will discuss the potential therapeutic use of agents that directly or indirectly block metabolism.
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.