ReviewTranslational oncology2025
PRMT5 inhibitors: Therapeutic potential in pancreatic 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 7 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
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Dietary sulforaphane in cancer chemoprevention: epigenetic regulation and PRMT5-MEP50 complex inhibition-a systematic review.Frontiers in pharmacology · 2026Pooled it
- Targeting PRMT5 Inhibitor-Induced Adaptation in Pancreatic Cancer with the RBM39 Degrader Indisulam.Cancer research communications · 2026Article
- Review
- DNA damage response inhibitors in pancreatic cancer: progress and challenges.Frontiers in oncology · 2026Review
- Cracking PRMT5: Mechanistic insights, clinical advances, and AI-driven strategies.Cancer letters · 2025Review
- Exploiting Synthetic Lethality of PRMT5 for Precision Treatment of MTAP-Deficient Glioblastoma.International journal of translational medicine (Basel, Switzerland) · 2025Article
- Epigenetic dysregulation in pancreatic cancer: emerging biomarkers and clinical applications.Frontiers in epigenetics and epigenomics · 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
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is predominantly driven by mutations in the Kirsten rat sarcoma virus (KRAS) oncogene. Due to the pivotal role of KRAS in PDAC pathogenesis, KRAS inhibitors (KRASi) have recently demonstrated initial signs of clinical efficacy. However, considering currently documented response rates and the resistance development to KRASi, additional targeted therapies are needed. In this context, we provide a summary of recent preclinical and clinical findings on protein arginine methyltransferase 5 (PRMT5) inhibitors (PRMT5i) and their implications for PDAC. PRMT5 has been linked to key oncogenic processes, including epithelial-mesenchymal transition (EMT), MYC and Hippo signaling pathways, glycolysis, and therapy resistance. With further advancements and optimization of PRMT5i-based therapies, these inhibitors hold significant potential as therapeutic agents for PDAC treatment. Therefore, we synthesize the current understanding of PRMT5i and highlight promising directions for future developments in PDAC.
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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.