ReviewCellular oncology (Dordrecht, Netherlands)2026
The histone acylation network: emerging therapeutic targets for remodeling the epigenetic landscape in pancreatic ductal adenocarcinoma.
Review in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
- Lactate-induced epithelial-mesenchymal transition: a metabolic nexus in pancreatic cancer metastasis.Translational cancer research · 2026Review
- Blocking L-carnitine synthesis by meldonium prolongs the survival in mice with pancreatic cancer.iScience · 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
8 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, a status primarily attributable to its intricate molecular circuitry. The histone acylation network serves as a key orchestrator of PDAC progression through epigenetic reprogramming, making its regulatory components high-value targets for groundbreaking therapeutic interventions. Here, we review how diverse histone acylations govern pancreatic cancer biology. We first outline the established roles of acetylation in proliferation, metastasis, and immune evasion. Subsequently, we focus on novel modifications intimately linked to tumor metabolic reprogramming, with a particular emphasis on histone lactylation. We also explore emerging modifications such as succinylation and propionylation as potential therapeutic targets. We further underscore that these diverse acylations exhibit extensive crosstalk, forming an intricate and dynamic regulatory network mediated by shared enzymatic “writers” and “erasers” (e.g., p300, HDACs), and exerting synergistic or antagonistic effects on key genes including MYC and GATA binding protein 6 (GATA6). By providing a comprehensive deciphering of the dysregulated histone acylation network, this review highlights its significant transformative potential. Such understanding not only unveils novel pathogenic drivers of pancreatic tumorigenesis but also establishes a mechanistic foundation for precision oncology. Furthermore, we evaluate the current landscape of clinical trials and discuss the potential of epigenetic agents to sensitize tumors to conventional or targeted therapies. By bridging the gap between complex molecular crosstalk and clinical application, this review aims to provide a practical framework for the rational design of targeted inhibitors and the formulation of synergistic combination therapies to overcome current treatment limitations and therapeutic resistance.
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Registered trials
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