ReviewTranslational oncology2025
Cyclin-dependent kinases as mediators of aberrant transcription in prostate cancer.
Review in Translational oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Tumor cell cycle regulation: integrated perspective of stage characteristics, regulatory networks, and signaling pathway intervention strategies.Molecular biomedicine · 2026Review
- Transcriptome Analysis, Machine Learning, and Experimental Identification of CDK7 Affecting the Progression of Pregnancy-induced Hypertension by Influencing Macrophage Polarization.Current molecular medicine · 2026Article
- Androgen receptor contributes to radioresistance through DNA repair and autophagy in AR-positive prostate cancer cells.bioRxiv : the preprint server for biology · 2025Article
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
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional control of gene expression is fundamental to all cellular processes. Conversely, transcriptional dysregulation is a hallmark of cancer. While this hallmark is a key driver of all malignancy-related process, it also represents a vulnerability that can be exploited therapeutically. Prostate cancer is a prime example of this phenomenon: it is characterised by aberrant transcription and treated with drugs that influence transcriptional pathways. Indeed, the primary oncogenic driver and therapeutic target of prostate cancer, the androgen receptor (AR), is a transcription factor. Moreover, a plethora of other transcriptional regulators, including transcriptional cyclin-dependent kinases (CDK7, CDK8 and CDK9), MYC and Bromodomain-containing protein 4 (BRD4), play prominent roles in disease progression. In this review, we focus on the roles of transcriptional CDKs in prostate cancer growth, metastasis and therapy resistance and discuss their interplay with AR, MYC and BRD4. Additionally, we explore recent advances in the therapeutic targeting of transcriptional CDKs and propose how these strategies could be effectively harnessed for the treatment of prostate cancer.
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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.