ReviewNature reviews. Clinical oncology2024
Targeting cuproplasia and cuproptosis in cancer.
Review in Nature reviews. Clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 225 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
225 citing papers in PubMed, 1 synthesis or guideline pooled it, 328 citations in OpenAlex.
- Cuproptosis as a therapeutic target in cancer: a Systematic Review and bibliometric analysis of the research landscape.Frontiers in oncology · 2025Pooled it
- GSH-responsive self-assembled nanoplatform synergistically enhances cuproptosis through metabolic reprogramming and oxidative stress amplification.Materials today. Bio · 2026Article
- Engineered bacteria reverses tumor cuproptosis resistance via cancer-associated fibroblast reprogramming for enhanced immunotherapy.Materials today. Bio · 2026Article
- Clinical translation and landscape of copper nanoparticles.Drug delivery and translational research · 2026Review
- Reprogramming the tumor microenvironment with oxygen-driven nanomotors for cuproptosis-enhanced immunotherapy.Materials today. Bio · 2026Article
- Penfluridol directly targets PDPK1 to suppress AKT1 phosphorylation and stabilize CTR1, inducing cuproptosis in colorectal cancer.Acta pharmacologica Sinica · 2026Article
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Cell death: immunogenic potential of cuproptosis in cancer.Signal transduction and targeted therapy · 2026Article
- Itaconate metabolism in regulated cell death.Molecular and cellular biochemistry · 2026Review
- A Self-Monitoring Single-Atom Copper Nanocapsule for Cascade-Responsive Tumor Cuproptosis Therapy.Angewandte Chemie (International ed. in English) · 2026Article
- A Domino-Synthesized Dicoordinate Copper(I) Bis-imidazopyridine Complex Triggering Cuproptosis/Ferroptosis for Enhanced Cancer Immunotherapy.Angewandte Chemie (International ed. in English) · 2026Article
- Subtype-Specific Alterations in Copper Trafficking Associated with KRAS Mutations in Isogenic Colorectal Cancer Cell Lines.Biological trace element research · 2026Article
- Unveiling the Impact of Copper Metabolism on Epithelial-Mesenchymal Transition of Triple-Negative Breast Cancer: Identification of Therapeutic Targets.Interdisciplinary sciences, computational life sciences · 2026Article
- Cuproplasia-associated LOXL2 cooperates withJournal of gastrointestinal oncology · 2026Article
- Current and future therapies for triple-negative breast cancer.Journal of hematology & oncology · 2026Review
- Cuproptosis: an emerging member of the immunogenic cell death family.Cell death and differentiation · 2026Article
- A cuproptosis-inducing covalent organic framework synergizes with oncolytic virus for tumor radiotherapy.Nature communications · 2026Article
- TPEN, a Well-Known Zinc Chelator, Sequesters Attomolar-Buffered Cellular Cu(I) Through an Oxygen-Dependent Mechanism.ACS chemical neuroscience · 2026Article
- EP300-Mediated MTF1-K218 Lactylation Buffers AR-Driven Copper Overload to Suppress Cuproptosis in Castration-Resistant Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
165 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
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper, an essential trace element that exists in oxidized and reduced forms, has pivotal roles in a variety of biological processes, including redox chemistry, enzymatic reactions, mitochondrial respiration, iron metabolism, autophagy and immune modulation; maintaining copper homeostasis is crucial as both its deficiency and its excess are deleterious. Dysregulated copper metabolism has a dual role in tumorigenesis and cancer therapy. Specifically, cuproplasia describes copper-dependent cell growth and proliferation, including hyperplasia, metaplasia and neoplasia, whereas cuproptosis refers to a mitochondrial pathway of cell death triggered by excessive copper exposure and subsequent proteotoxic stress (although complex interactions between cuproptosis and other cell death mechanisms, such as ferroptosis, are likely and remain enigmatic). In this Review, we summarize advances in our understanding of copper metabolism, the molecular machineries underlying cuproplasia and cuproptosis, and their potential targeting for cancer therapy. These new findings advance the rapidly expanding field of translational cancer research focused on metal compounds.
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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.