ArticleActa materia medica2025
PROTAC technology for prostate cancer treatment.
Article in Acta materia medica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Therapeutic potentials of curcumin in prostate cancer: a comprehensive review of pathways and clinical prospects.Prostate international · 2026Review
- International standards and good practice guidelines in traditional, complementary and integrative medicine: a scoping review.Frontiers in pharmacology · 2026Article
- PROTAC Technology as a New Tool for Modern Pharmacotherapy.Molecules (Basel, Switzerland) · 2025Review
- PROTAC: a revolutionary technology propelling small molecule drugs into the next golden age.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Prostate cancer (PrCa) is the most prevalent urogenital cancer in men, marked by uncontrolled cellular growth that leads to abnormal enlargement of the prostate gland. The metastatic spread of PrCa is the primary cause of mortality, causing cancer cells disseminate to distant sites, such as bones, the pelvis, and other organs. Key contributors to PrCa progression include genetic mutations, elevated androgen receptor (AR) expression, gene amplification, and the rise of AR splice variants. Although androgen deprivation therapy (ADT) remains the mainstay for early-stage PrCa treatment, its efficacy is rather temporary, as many cases advance to castration-resistant PrCa (CRPC), presenting a significant therapeutic hurdle. This review explores key biomarkers for PrCa and the latest therapeutic strategies for CRPC, with a particular focus on the innovative Proteolysis-targeting chimera (PROTAC) technology. This approach offers a novel means of degrading target proteins, and we discuss how PROTACs hold potential as effective strategies to combat resistance mechanisms in CRPC.
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.