ReviewJournal of experimental & clinical cancer research : CR2025
Balancing between cuproplasia and copper-dependent cell death: molecular basis and clinical implications of ATOX1 in cancer.
Review in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Copper, cuproptosis, and cancer: biology concepts of a novel cell death.Apoptosis : an international journal on programmed cell death · 2026Review
- Balancing cellular copper levels via the post-translational regulation of copper transport.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- ATP7A Orchestrates Tumor Progression and Cuproptosis in Hepatocellular Carcinoma via the LINC02038-miR-506-3p Regulatory Circuit.Journal of biochemical and molecular toxicology · 2026Article
- Targeting Copper in Cancer: Chelators to Counteract Cuproplasia and Ionophores to Promote Cuproptosis.Journal of medicinal chemistry · 2026Review
- Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.Journal of hematology & oncology · 2026Review
- From copper imbalance to immunometabolic remodeling: cuproptosis-related vulnerability and therapeutic hypotheses in autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- In Vitro Radiobiological Evaluation of [Pharmaceuticals (Basel, Switzerland) · 2026Article
- Integrative gene ontology-driven analysis of the eutopic endometrium reveals key dysregulated functionomes and pathways in endometriosis.Journal of the Chinese Medical Association : JCMA · 2026Article
- Atox1 promotes CRC progression by protecting DNA damage through interacts with a novel copper-binding protein PARP1.Cell communication and signaling : CCS · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Copper dyshomeostasis and cardiovascular disease: Molecular mechanisms and new strategies for targeted intervention with cuproptosis (Review).International journal of molecular medicine · 2026Review
- Cuproptosis and prostate cancer: from molecular mechanisms and microenvironment remodeling to precision therapy.Frontiers in oncology · 2026Review
- Cisplatin resistance in ovarian cancer: exploration and insights from metal ion homeostasis imbalance.Frontiers in cell and developmental biology · 2026Review
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.
Funding
Abstract
Human antioxidant protein 1 (ATOX1) is an essential regulator of copper homeostasis in cells. By interacting with other proteins involved in controlling the intracellular levels of cuprous ions (Cu
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.