Evidence mapPaperPMID 42288694Full record

ReviewCancer gene therapy2026

Hepatitis B virus-induced hepatocellular carcinoma: HBx-associated epigenetic mechanisms and therapeutic opportunities.

Atahar Husein, Azfar Jamal, Mohammad Azhar Kamal, Yaser E Alqurashi, Esam S Al-Malki, Mohammed M Naiyer, Syed Arif Hussain, Mohiuddin Khan Warsi

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In one paragraph

Review in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Atahar Husein *Department of Biotechnology, Jamia Millia Islamia, New Delhi, India.
Azfar Jamal *Department of Biology, College of Science Al-Zulfi, Majmaah University, Al-Majmaah, Saudi Arabia. azfarjamal@mu.edu.sa.ORCID http://orcid.org/0000-0002-4671-4995
Mohammad Azhar KamalDepartment of Pharmaceutics, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Alkharj, Saudi Arabia.
Yaser E AlqurashiDepartment of Biology, College of Science Al-Zulfi, Majmaah University, Al-Majmaah, Saudi Arabia.
Esam S Al-MalkiDepartment of Biology, College of Science Al-Zulfi, Majmaah University, Al-Majmaah, Saudi Arabia.
Mohammed M NaiyerDept. of Pharmaceutics, UCL School of Pharmacy, University College London, London, UK.
Syed Arif HussainRespiratory Care Department, College of Applied Sciences, Almaarefa University, Riyadh, Saudi Arabia.
Mohiuddin Khan WarsiDepartment of Biochemistry, College of Science, University of Jeddah, Jeddah, Saudi Arabia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hepatitis B virus (HBV) infection is a major etiological factor in the development of hepatocellular carcinoma (HCC), a cancer that causes a large number of cancer-related deaths around the world. Although antiviral treatments are effective, the risk of HCC remains because studies using advanced sequencing have shown that liver cells still carry integrated viral DNA, experience ongoing inflammation, and undergo lasting changes in epigenetic regulation. HBV maintains its genome in liver cells as a chromatin-like cccDNA structure, and with the help of the HBx protein, it manipulates the cell's chromatin machinery to support viral gene expression and disrupt normal control of enhancers, DNA methylation, and Polycomb regulation. These alterations enhance transcriptional plasticity and, in the context of chronic liver injury and additional somatic mutations, may contribute to malignant transformation. This review highlights recent mechanistic studies that have suggested a pathway linking HBV persistence to chromatin dysfunction. Further, it outlines an emerging therapeutic opportunity with chromatin-directed drugs, as well as rational combinations of these drugs with immunotherapy for HBV-related HCC.

Indexed as

Carcinoma, HepatocellularEpigenesis, GeneticHepatitis B, ChronicHepatitis B virusLiver NeoplasmsTrans-ActivatorsAnimalsHumansViral Regulatory and Accessory Proteinshepatitis B virus X proteinTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

What Socratic holds

Textmetadata
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Registered trials

None linked

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.