ArticleJHEP reports : innovation in hepatology2025
Identification and clinical implications of endogenous retrovirus elements suppressed by SETDB1 in hepatocellular carcinoma.
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Histone methyl-transferase G9a inhibition boosts the efficacy of immune checkpoint inhibitors in experimental hepatocellular carcinoma.Cell reports. Medicine · 2026Article
- Activation of endogenous retroviruses in tumor cells and their immunomodulatory mechanisms: from molecular basis to clinical translation.Frontiers in oncology · 2026Review
- Endogenous retroviruses and response to immune checkpoint inhibitors: mechanisms, clinical evidence, and therapeutic implications.Frontiers in immunology · 2026Review
- Multi-omic analysis of hepatocellular carcinoma reveals aberrant cis-regulatory changes and dysregulated retrotransposons with prognostic potential.Communications biology · 2025Article
- Endogenous and exogenous viral reactivation as a driver of epigenetic drift and mitophagy failure in aging.Biogerontology · 2025Review
- Article
Corrections and comments
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background & Aims: The inhibition of epigenetic regulators activates endogenous retrovirus (ERV) expression, which can stimulate a viral mimicry response in cancer cells. ERV elements are aberrantly expressed in hepatocellular carcinoma (HCC); however, the expression of ERVs regulated by histone modifications and their clinical significance in HCC remain unclear. Here, we identified specific human endogenous retrovirus (HERV) elements epigenetically suppressed by the histone methyltransferase SETDB1 in HCC. Methods: The Cancer Genome Atlas (TCGA) dataset was analyzed to identify HERV elements based on Results: TCGA analysis revealed an inverse correlation between Conclusions: The suppression of four novel HERV elements by SETDB1 serves as a prognostic marker in HCC. Activation of these SETDB1-regulated HERVs could represent a promising therapeutic strategy for HCC. Impact and implications: An inverse relationship between retroelements including human endogenous retrovirus (HERV) elements and
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Registered trials
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