ReviewCell death & disease2025
Resistance of first-line targeted drugs in hepatocellular carcinoma: the epigenetic regulation mechanisms.
Review in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- SERPINE2-mediated activation of JAK2/STAT3 facilitates NRF2 nuclear translocation and GCLC transcription to confer ferroptosis resistance and lenvatinib resistance in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Engineering Selenium-Chitosan Nanoparticles for Enhanced Hepatic Delivery of Sunitinib and Improved In Vitro Anticancer Activity in Hepatocellular Carcinoma Models.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The lncRNA-DNA Methylation Axis in Hepatocellular Carcinoma: Mechanisms, Epigenetic Plasticity, and Biological Implications.Biology · 2026Review
- Lysosome-dependent cell death in hepatocellular carcinoma: unlocking the therapeutic potential of natural products.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Targeted therapy has revolutionized the treatment landscape of hepatocellular carcinoma (HCC), offering unprecedented hope to patients. However, despite its promise, significant challenges arise in the form of drug resistance. Only a fraction of HCC patients respond to targeted therapy, and even those who respond often develop resistance over time. Sorafenib and lenvatinib, the sole first-line targeted therapeutic drugs for HCC, face severe clinical limitations due to drug resistance. Understanding the mechanisms underlying sorafenib/lenvatinib resistance is crucial for maximizing treatment efficacy. Recent studies have highlighted the pivotal role of epigenetic regulation in drug resistance. Cancer is recognized as both a genetic and epigenetic disease, with epigenetic factors influencing various aspects of tumor cell biology, especially drug resistance. This review systematically summarizes the mechanisms of epigenetic-mediated sorafenib/lenvatinib resistance, encompassing non-coding RNA (ncRNA) regulation, DNA methylation, RNA methylation, and histone modification. These abnormal epigenetic processes typically influence biological activities, including escaped programmed cell death, tumor metabolic reprogramming, formation and maintenance of drug-resistant cells, uncontrolled cell proliferation signaling pathways, and abnormal transport processes, ultimately culminating in profound drug resistance. By comprehensively summarizing the latest discoveries in epigenetic regulation mechanisms, this review highlights potential strategies to overcome drug resistance, paving the way for future advancements in HCC treatment.
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What Socratic 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 Socratic graph.