Evidence map›Paper›PMID 42053692›Full record

ReviewMolecular biology reports2026

Beyond silencing: integrative multi-omics and spatial profiling unravel the systems-level role of piRNAs in HBV-driven Hepatocarcinogenesis.

A Zainb, Farag M A Altalbawy, Shahad Mohammed Dhiaa Younis, Sundus Mohammed Ali Al-Bazi, Ahmed Adnan Eiada, Salah Hassan Zain Al-Abdeen, Muyassar Norberdiyeva, Aseel Smerat

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

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0cells of the map it votes in
0citing papers in PubMed
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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.

A ZainbDepartment of medical analysis, Medical laboratory technique college, The Islamic University, Najaf, Iraq.
Farag M A AltalbawyDepartment of Chemistry, University College of Duba, University of Tabuk, Tabuk, Saudi Arabia. f_altalbawy@yahoo.com.
Shahad Mohammed Dhiaa YounisCollege of Pharmacy, Alnoor University, Mosul, Iraq.
Sundus Mohammed Ali Al-BaziPreventive dentistry, College of Dentistry, Al-zahrawi University, Karbala, Iraq.
Ahmed Adnan EiadaAl-Farahidi University, Baghdad, Iraq.
Salah Hassan Zain Al-AbdeenDepartment of Medical Laboratories Technology, Al-Nisour University College, Nisour Seq. Karkh, Baghdad, Iraq.
Muyassar NorberdiyevaDepartment of Chemistry and Its Teaching Methods,, National Pedagogical University of Uzbekistan, Tashkent, Uzbekistan.
Aseel SmeratFaculty of Educational Sciences, Al-Ahliyya Amman University, Amman, 19328, Jordan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) driven by chronic hepatitis B virus (HBV) infection remains a global health challenge, with late diagnosis and limited therapeutic options underscoring the need for novel biomarkers and mechanistic insights. Once considered guardians of the germline, PIWI-interacting RNAs (piRNAs) are now emerging as key somatic regulators of chromatin, transcription, and signaling in cancer. This review considers HBV a plausible perturbant of the hepatic piRNA ecosystem, through viral integration, epigenetic remodeling, and altered intercellular communication. Unlike prior reviews that mainly catalog PIWI/piRNA findings in HCC or summarize broader liver-cancer multi-omics, this article advances a testable HBV-piRNAome disruptor model with three falsifiable predictions: HBV integration and 3D genome rewiring alter piRNA-cluster output, HBx/HBsAg-driven chromatin remodeling shifts PIWI/piRNA stoichiometry, and spatially restricted tumor, stromal, and immune niches generate distinct piRNA signatures that can be mapped in matched tissue and plasma. This framework is intended to help move from association to testable mechanism and, where supported, to clinically anchored validation. This is a conceptual narrative review rather than a systematic review or meta-analysis; therefore, no PRISMA flow diagram is provided, and the cited literature was selected for conceptual and mechanistic relevance. We argue that decoding HBV-driven hepatocarcinogenesis requires linking piRNA dysregulation to the biological consequences of HBV integration, HBx-driven epigenetic remodeling, and niche-specific fibrogenic and immune reprogramming; spatial multi-omics should be used to localize these mechanisms to the relevant cell types and tissue compartments. Such systems-level profiling can help nominate candidate biomarkers and therapeutic vulnerabilities for future validation, but clinical translation will still require prospective cohorts, standardized EV/small-RNA workflows, rigorous functional confirmation, and formal safety/regulatory review before use in patients.

Indexed as

Carcinoma, HepatocellularHepatitis B, ChronicHepatitis B virusLiver NeoplasmsPiwi-Interacting RNARNA, Small InterferingAnimalsCarcinogenesisHumansMultiomicsVirus IntegrationPiwi-Interacting RNARNA, Small InterferingHepatitis B virusHepatocellular carcinomaMulti-omicspiRNAsSpatial profiling

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Registered trials

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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.