ArticleApoptosis : an international journal on programmed cell death2025
A novel programmed cell death signature predicts clinical outcomes in clear cell renal cell carcinoma and identifies PLK1 as a therapeutic target.
Article in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clear-cell renal cell carcinoma (ccRCC) remains therapeutically challenging despite recent treatment advances. Here, we analyzed 18 distinct programmed cell death (PCD) patterns across multiple cohorts and developed a novel prognostic scoring system (PCDscore) based on eight PCD-related genes. We established an eight-gene signature that demonstrated robust predictive capability and, when integrated with clinical staging, yielded a nomogram with strong performance across independent cohorts. High PCDscore groups exhibited enhanced immunosuppressive features, while low PCDscore groups showed better immunotherapy responses. Single-cell analysis of 54,166 cells revealed activation of multiple oncogenic pathways in high PCDscore tumor cells, along with extensive intercellular communication networks. To further investigate the role of PLK1, we identified 282 co-expressed genes and conducted functional enrichment analyses, revealing its significant association with pathways such as the cell cycle and NF-κB signaling. A protein-protein interaction (PPI) network and Bayesian network analysis highlighted PLK1 as a key regulator of PKMYT1, with CDC20 and CCNB2 acting upstream. Functional validation confirmed PLK1, the highest weighted gene in our signature, significantly influences tumor progression in ccRCC. This study establishes a reliable prognostic scoring system and identifies PLK1 as a potential therapeutic target, providing valuable clinical guidance for treatment decision-making in ccRCC patients.
Indexed as
Identifiers
40488834What 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.