Evidence map›Paper›PMID 39743539›Full record

ArticleJournal of biomedical science2025

HBV DNA integration and somatic mutations in HCC patients with HBV-HCV dual infection reveals profiles intermediate between HBV- and HCV-related HCC.

Chiao-Ling Li, Chia-Lang Hsu, You-Yu Lin, Ming-Chih Ho, Rey-Heng Hu, Sheng-Tai Tzeng, Ya-Chun Wang, Yasuhito Tanaka, Pei-Jer Chen, Shiou-Hwei Yeh

Abstract read
In one paragraph

Article in Journal of biomedical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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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

2 citing papers in PubMed.

  1. Article
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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

10 authors.

Chiao-Ling LiGraduate Institute of Microbiology, National Taiwan University College of Medicine, Taipei, Taiwan.
Chia-Lang HsuDepartment of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
You-Yu LinGraduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.
Ming-Chih HoDepartment of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
Rey-Heng HuDepartment of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
Sheng-Tai TzengTCM Biotech International Corp., Taipei, Taiwan.
Ya-Chun WangTCM Biotech International Corp., Taipei, Taiwan.
Yasuhito TanakaDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
Pei-Jer ChenGraduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan. peijerchen@ntu.edu.tw.ORCID http://orcid.org/0000-0001-8316-3785
Shiou-Hwei YehGraduate Institute of Microbiology, National Taiwan University College of Medicine, Taipei, Taiwan. shyeh@ntu.edu.tw.

Funding

Ministry of Education NTU-113L901401National Science and Technology Council 113-2326-B-002-001-National Science and Technology Council 113-2326-B-002-002-
6 · The paper itself

Abstract

backgroundIn regions with a high prevalence of chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, coinfected patients face a heightened risk of developing hepatocellular carcinoma (HCC), termed HBV/HCV-related HCC (HBCV-HCC). We aimed to investigate the contribution of preexisting chronic hepatitis B (CHB) and subsequent chronic hepatitis C (CHC) to the development of HBCV-HCC.

methodsWe examined HBV's involvement in 93 HBCV-HCC cases by analyzing HBV DNA integration as an indicator of HCC originating from HBV-infected hepatocytes, compared with 164 HBV-HCCs and 56 HCV-HCCs as controls.

resultsNext generation sequencing revealed that 55% of HBCV-HCCs exhibited clonal HBV integration, which falls between the rates observed in HBV-HCCs (88%) and HCV-HCCs (7%), with similar integration patterns to HBV-HCCs. Common HCC somatic mutation analysis indicated HCV superinfection in HBCV-HCCs correlated with increased mutation rates in the telomerase reverse transcriptase (TERT) promoter and beta-catenin genes. Transcriptome analysis showed a prevalence of replicating HCV over HBV in HBCV-HCCs, with preexisting HBV exerting a proliferative role. The comparison of clinical characteristics revealed similarities between HBCV-HCC and HCV-HCC patients, including later onset for HBCV-HCC, possibly due to HCV superinfection slowing carcinogenesis. Notably, HBCV-HCCs with the same driver mutation, HBV integration at the TERT promoter, tended to develop later and showed a better prognosis post-tumor resection than HBV-HCCs.

conclusionsOur findings shed light on the interplay between preexisting CHB and subsequent CHC in elevating the risk of HBCV-HCC. These insights are crucial for understanding viral etiology-specific carcinogenesis and guiding surveillance policies for HBCV-HCC post-antiviral therapy.

Indexed as

Carcinoma, HepatocellularHepatitis B, ChronicHepatitis B virusLiver NeoplasmsMutationAdultAgedCoinfectionDNA, ViralFemaleHepacivirusHepatitis C, ChronicHumansMaleMiddle AgedVirus IntegrationDNA, ViralHepatitis B virusHepatitis C virusHepatocellular carcinoma

Identifiers

PMID39743539
PMCPMC11694426

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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.