ArticleHuman mutation2026
A Cuproptosis-Glycolysis Signature Predicts Prognosis and Highlights AURKA as a Therapeutic Target in ccRCC.
Article in Human mutation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Integrating machine learning, deep learning, and docking to predict aristolochic acid A carcinogenesis.Frontiers in pharmacology · 2026Article
- A Cuproptosis-Glycolysis Signature Predicts Prognosis and Highlights AURKA as a Therapeutic Target in ccRCC.Human mutation · 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cuproptosis, a recently identified form of cell death, is closely linked to glycolysis; however, the mechanistic interplay between these processes in clear cell renal cell carcinoma (ccRCC) remains to be fully elucidated. Utilizing data from the TCGA and CPTAC databases, we developed and validated a cuproptosis-glycolysis-related gene (CuG) scoring model to investigate its associations with clinical outcomes, tumor immune infiltration, immunotherapy response, and drug sensitivity. Our analysis established a robust 10-gene risk model with significant prognostic value that effectively stratifies ccRCC patients into distinct high- and low-risk groups exhibiting marked differences in clinical profiles and therapeutic responses. Through integrated bioinformatic analyses alongside in vitro and in vivo experimental validation, we identified AURKA as a key functional regulator within this signature. Beyond promoting tumor cell proliferation, migration, and invasion, AURKA may have a significant role in modulating antitumor immunity. Collectively, by establishing a clinically applicable prognostic scoring system and nominating AURKA as a potential therapeutic target, our study offers translational implications for treatment decision-making in ccRCC.
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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.