ReviewInternational journal of cancer2025
Rewriting the MASLD-associated hepatocellular carcinoma script: Targeting epigenetics and metabolism.
Review in International journal of cancer, 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
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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
4 citing papers in PubMed.
- Multi-scale computational analysis of monoacylglycerol lipase inhibition as a new therapeutic strategy for hepatocellular carcinoma.Scientific reports · 2026Article
- β-Hydroxybutyrate upregulates hepatic histone β-hydroxybutyrylation modification, promotes the expression of PPARα, and alleviates the hepatic steatosis in MASLD.Clinical epigenetics · 2026Article
- Epigenetic reprogramming in metabolic dysfunction-associated steatotic liver disease: from metabolic memory to precision medicine.Frontiers in physiology · 2026Review
- Rewriting the MASLD-associated hepatocellular carcinoma script: Targeting epigenetics and metabolism.International journal of cancer · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal epigenetic patterns are crucial for the progression of metabolic-associated steatotic liver disease (MASLD) and hepatocellular carcinoma (HCC) development. Recent research focused on the interplay between epigenetics and altered metabolic pathways in HCC from MASLD, suggesting that the reversibility of epigenetic changes offers potential for new therapeutic strategies. However, identifying effective epigenetic targets remains challenging due to the diverse etiologies of HCC. Targeting metabolic reprogramming, MASLD-associated HCC shows promise in reducing lipid anabolism. In this context, a more comprehensive understanding of metabolomic changes closely tied to druggable epigenetic modifications is of utmost importance. This review provides a concise summary of the key factors driving hepatocarcinogenesis in MASLD and delves deeper into the epigenetic mechanisms. Finally, we aim to present an overview of the primary mechanisms concerning the intricate bidirectional interplay between the metabolome and epigenetic modifications in MASLD-associated HCC, along with therapeutic strategies specifically targeting epigenetics and metabolomic alterations.
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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.