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HCC Associated with Viral Liver Infections (HBV, HCV, and HDV) and Other Rare Conditions

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Infectious Agents and Cancer".

Deadline for manuscript submissions: 11 December 2026 | Viewed by 762

Special Issue Editors


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Guest Editor
Medical Professional Academic Role, Department of Medicine-DIMED, University of Padua, 35128 Padova, Italy
Interests: clinical and epidemiological features of chronic hepatitis C and B and its antiviral treatments; cirrhosis and complication of evolutive liver disease; natural history and treatment of hepatocellularcarcinoma; transient elastography for staging of chronic liver diseases; cardiac cirrhosis; Fontan associate liver disease
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Internal Medicine & Hepatology Unit, University-Hospital of Padua, 35128 Padova, Italy
Interests: clinical and epidemiological aspects of chronic hepatitis viral infections (HCV, HBV, HDV), high degree specialization on transient elastography staging of liver diseases in the setting of various etiologies (from viral agents to Metabolic associated steatotic liver disease, MASLD, and Fontan associated liver disease, FALD, and other rare liver vascular conditions determining liver injury)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver and represents a major global health burden. It is currently a leading cause of cancer-related mortality worldwide, particularly in regions with a high prevalence of chronic hepatitis B virus (HBV), hepatitis C virus (HCV), and coinfections with HBV and HCV or with HBV and hepatitis D virus (HDV). However, HCC may also arise from numerous other etiological factors capable of inducing hepatocarcinogenesis. The development of HCC is typically the result of a multistep process involving chronic liver injury, persistent inflammation, oxidative stress, and compensatory regeneration, ultimately leading to cirrhosis, a key predisposing condition.

The aim of this Special Issue is to advance understanding of the epidemiology, etiopathogenesis, diagnostic approaches, and therapeutic strategies related to HCC associated with viral infections (HBV, HCV, and HDV), with the overarching goal of improving patient outcomes through earlier diagnosis and optimized clinical management. Original research articles presenting novel laboratory data and clinical evidence elucidating the pathogenesis, progression, or therapeutic targets of HCC are strongly encouraged. This includes mechanistic and translational studies conducted in cohorts with hepatitis virus infections (HCV, HBV, and HDV) known to drive HCC development, as well as in individuals exposed to hepatotoxic risk factors (e.g., alcohol, PHAS, drugs, and steatosis) that predispose to HCC. Submissions addressing other chronic liver conditions that act as key precancerous lesions for HCC are also welcome, including chronic cholestasis (e.g., PBS, PBC, and congenital defects of bile transporters) and vascular or congestive liver diseases (e.g., congenital heart disease-associated liver disease, Fontan-associated liver disease, Budd–Chiari syndrome, and portosystemic shunts).

Dr. Liliana Chemello
Dr. Luisa Cavalletto
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hepatocellular carcinoma
  • viral infections
  • hepatocarcinogenesis
  • chronic liver damage
  • epidemiology
  • etiopathogenesis
  • diagnostic approaches
  • therapeutic strategies

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Published Papers (1 paper)

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Research

19 pages, 3720 KB  
Article
Alpha-1B Glycoprotein Is a Novel Hepatocyte-Derived Host Factor Associated with In Vitro Inhibition of HBV Replication and Hepatocellular Carcinoma Progression
by Juan Lyu, Takuto Nosaka, Yosuke Murata, Yu Akazawa, Tomoko Tanaka, Kazuto Takahashi, Tatsushi Naito, Masahiro Ohtani, Lihong Zhang and Yasunari Nakamoto
Cancers 2026, 18(4), 662; https://doi.org/10.3390/cancers18040662 - 18 Feb 2026
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Abstract
Background: Chronic hepatitis B virus (HBV) infection is a major risk factor of hepatocellular carcinoma (HCC), and hepatocyte-derived host factors play important roles in HBV-associated tumor progression. Alpha-1B glycoprotein (A1BG) is a plasma glycoprotein reported to be dysregulated in multiple cancers. In this [...] Read more.
Background: Chronic hepatitis B virus (HBV) infection is a major risk factor of hepatocellular carcinoma (HCC), and hepatocyte-derived host factors play important roles in HBV-associated tumor progression. Alpha-1B glycoprotein (A1BG) is a plasma glycoprotein reported to be dysregulated in multiple cancers. In this study, we investigated the functional role of A1BG in HBV-associated HCC progression. Methods: Both the HepG2 and HBV-transfected HepG2 cell lines were used to examine the biological effects of A1BG. A1BG expression was modulated using siRNA and a plasmid vector. A series of functional assays were conducted to assess cell proliferation, apoptosis, stemness, migration, and invasion. RNA microarray analysis and gene set enrichment analysis (GSEA) were performed to identify A1BG-regulated pathways. Results: Functionally, A1BG overexpression suppressed cell proliferation, stemness, migration, invasion, and HBV products while promoting apoptosis in both HepG2 and HBV-transfected HepG2 cells. In contrast, opposite effects were shown in the event of A1BG knockdown. Moreover, A1BG expression was reduced in HBV-associated HCC tissues and correlated with advanced pathological stage and poor prognosis. RNA microarray analysis and GSEA revealed the activation of anti-HBV-related genes and suppression of FGFR1 signaling and the matrix metalloproteinase pathway in A1BG-overexpressing cells. Conclusions: This study provides evidence that A1BG may be a novel host factor associated with the in vitro suppression of HBV replication and HCC progression by modulating pathways related to enhanced antiviral effects, reduced proliferative capacity and stemness, and suppression of EMT. These findings suggest that A1BG is a potential therapeutic target in HBV-related HCC. Full article
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