ReviewCell death discovery2025
Decoding cuproptosis and cuproplasia: implications for therapeutic strategies in renal cell carcinoma.
Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Interaction of HIF-1a with various cell death pathways in tumor immune microenvironment (TIME).Apoptosis : an international journal on programmed cell death · 2026Pooled it
- Dihydrolipoamide dehydrogenase promotes hepatocellular carcinoma progression and modulates cuproptosis-dependent cell death.Functional & integrative genomics · 2026Article
- KIF7 promotes the proliferation of clear cell renal cell carcinoma by activating the WNT/β-catenin signaling pathway.Clinical and experimental medicine · 2026Article
- Copper homeostasis and cuproptosis in cancer: mitochondrial metabolic dependency and nanomedicine-based therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- RGS19 drives tumor progression and immunosuppression in clear cell renal cell carcinoma by modulating CAMs and EMT.World journal of surgical oncology · 2026Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal cell carcinoma (RCC) is one of the primary drivers of cancer-related mortality worldwide. Despite advancements in cancer diagnosis and management, there is a lack of effective available treatment options for such patients. This is often attributed to late diagnosis, lack of biomarkers, and resistance against standard-of-care therapies. Thus, identifying novel targets in RCC is needed to improve disease outcomes. Cu is a trace element required for homeostasis, and its dysregulation is linked to cancer. Cuproptosis, a programmed cell death, occurs due to intracellular Cu overload, disrupting the TCA cycle, inducing oxidative stress, and impairing metabolism. In cancer, abnormal Cu levels drive Cu-dependent proliferation, termed cuproplasia. The role of cuproptosis and cuproplasia in RCC remains unclear; their comprehensive understanding will enable the discovery of novel targets for effective therapy. This review explores their molecular mechanisms, impact on RCC progression, and therapeutic potential.
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.