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Cancers
Special Issues
Hepatitis Viruses and Cancer
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Hepatitis Viruses and Cancer

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

Deadline for manuscript submissions: closed (1 November 2024) | Viewed by 3897

Special Issue Editors

Prof. Dr. John Koskinas

E-Mail Website
Guest Editor
Department of Medicine, National and Kapodistrian University of Athens, Medical School, Hippokration General Hospital of Athens, Athens, Greece
Interests: hepatocellular caricinoma; viral hepatitis (HBV/HCV); liver diseases
Dr. Urania Georgopoulou

E-Mail Website
Guest Editor
Department of Microbiology, Laboratory of Molecular Virology, Pasteur Institute, Athens, Greece
Interests: viral hepatitis; HCV; HBV; hepatocellular carcinoma; molecular virology

Special Issue Information

Dear Colleagues,

Liver cancer is a major health problem and hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Hepatitis viruses (HBV and HCV) have been identified between the major etiologies of HCC. HBV and HCV are non-cytopathic viruses that develop mechanisms of escape from immunological control with functional defects of virus-specific T-cell response. This allows them to persist and cause chronic hepatic inflammation, thus leading to cirrhosis and the development of HCC.

One major reason for the failure of HBV treatment is the inability to eradicate covalently closed viral circular DNA (cccDNA), which is a stable episomal form of the viral genome. Epigenetic modifications of cccDNA contribute to viral replication and the outcome of chronic HBV infection. Moreover, HBV integration into host genome contributes to carcinogenesis, even in the absence of cirrhosis. The current antiviral drugs improve the overall patient outcomes through the effective suppression of viral replication, but they do not eradicate the cccDNA, which often causes viral reactivation after the cessation of treatment.

HCV infection is a common form of chronic viral hepatitis worldwide, particularly in high-risk populations, leading to cirrhosis and HCC. The contributing mechanisms to the development of liver cancer are oxidative and ER stress, TGF-induced EMT, steatosis and insulin resistance. The availability of DAAs has revolutionized the treatment of patients with chronic HCV with their ability to target the virus. However, patients with cirrhosis remain at risk for HCC development after successful treatment. Furthermore, the identification and treatment of HCV carriers at an early stage in certain high-risk groups is a challenge for national health systems.

In this Special Issue, we wish to publish original research articles and reviews that aim to delineate cellular, molecular and epigenetic research on liver cancer caused by hepatitis viruses. Epidemiological and clinical research articles are also welcome based on results from various viewpoints.

Prof. Dr. John Koskinas
Dr. Urania Georgopoulou
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

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

  • viral hepatitis
  • hepatocellular carcinoma
  • HBV
  • HCV
  • HCC pathogenesis

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Published Papers (3 papers)

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Research

11 pages, 1911 KiB  
Article
Hepatitis B Virus-Induced Resistance to Sorafenib and Lenvatinib in Hepatocellular Carcinoma Cells: Implications for Cell Viability and Signaling Pathways
by Narmen Esmael, Ido Lubin, Ran Tur-Kaspa and Romy Zemel
Cancers 2024, 16(22), 3763; https://doi.org/10.3390/cancers16223763 - 8 Nov 2024
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Abstract
Background/Objectives: Sorafenib and lenvatinib are tyrosine kinase inhibitors used in hepatocellular carcinoma (HCC) treatment. This study investigates how hepatitis B virus (HBV) infection affects their efficacy in HepG2 hepatoma cells. Methods: HepG2 and HBV-infected HepG2/2215 cells were treated with varying concentrations [...] Read more.
Background/Objectives: Sorafenib and lenvatinib are tyrosine kinase inhibitors used in hepatocellular carcinoma (HCC) treatment. This study investigates how hepatitis B virus (HBV) infection affects their efficacy in HepG2 hepatoma cells. Methods: HepG2 and HBV-infected HepG2/2215 cells were treated with varying concentrations of both drugs. The cell viability, cell cycle gene expression, cycle progression, and phosphorylation levels of ERK and AKT were analyzed. Results: The HBV-infected cells showed significant alterations in their cell cycle gene expressions, with an 80-fold increase in CCND2 expression and a higher proportion of cells in the G2/M phase, indicating enhanced proliferation. While both drugs decreased HepG2 cell viability in a concentration-dependent manner, HBV infection conferred resistance, as evidenced by the increased viable cells in the HepG2/2215 cultures. Sorafenib and lenvatinib decreased key cyclin and cyclin-dependent kinase expressions in uninfected cells, with less effect on the HBV-infected cells. Both drugs lowered the pERK and pAKT levels in the HepG2 cells. In the HBV-infected cells, sorafenib reduced the pERK and pAKT levels to a lesser extent. However, treatment with lenvatinib elevated the levels of pERK and pAKT. Conclusions: In conclusion, HBV infection increases resistance to both sorafenib and lenvatinib in hepatoma cells by influencing the cell cycle regulatory genes and critical signaling pathways. However, the resistance mechanisms likely differ between the two medications. Full article
(This article belongs to the Special Issue Hepatitis Viruses and Cancer)
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14 pages, 2572 KiB  
Article
Effect of Direct Acting Antiviral Drugs on the Occurrence and Recurrence of Intra- and Extra-Hepatic Malignancies in Patients with Chronic Hepatitis C Virus Infection
by Pompilia Radu, Chiara Becchetti, Jonas Schropp, Patrick Schmid, Patrizia Künzler-Heule, Joachim Mertens, Darius Moradpour, Beat Müllaupt, David Semela, Francesco Negro, Markus Heim, Olivier Clerc, Maroussia Roelens, Olivia Keiser, Annalisa Berzigotti and Swiss Hepatitis C Cohort Study
Cancers 2024, 16(14), 2573; https://doi.org/10.3390/cancers16142573 - 18 Jul 2024
Cited by 1 | Viewed by 1071
Abstract
Introduction: The use of direct-acting antivirals (DAAs) has drastically changed the management of HCV-infected patients by achieving a 95–98% sustained virologic response (SVR) and reducing morbidity and mortality in this population. However, despite their effectiveness, controversy exists concerning the occurrence of oncologic events [...] Read more.
Introduction: The use of direct-acting antivirals (DAAs) has drastically changed the management of HCV-infected patients by achieving a 95–98% sustained virologic response (SVR) and reducing morbidity and mortality in this population. However, despite their effectiveness, controversy exists concerning the occurrence of oncologic events following DAA therapy. Aims and Methods: A retrospective analysis was conducted on data from the Swiss Hepatitis C Cohort Study, a prospective cohort involving patients with positive HCV viremia upon inclusion, enrolled in various Swiss centers from September 2000 to November 2021. To examine potential differences in the risk of intrahepatic tumor (IHT) occurrence and death among patients treated with direct-acting antivirals (DAAs), untreated patients, and those receiving interferon (IFN)-based therapy, a semiparametric competing risk proportional hazards regression model was used. Results: Among 4082 patients (63.1% male, median age 45 years; genotype 1: 54.1%; cirrhosis: 16.1%), 1026 received exclusive treatment with IFN-based regimens, and 1180 were treated solely with DAAs. Over a median follow-up of 7.8 years (range: 3.8–11.9), 179 patients (4.4%) developed intrahepatic tumors (IHT), and 168 (4.1%) experienced extrahepatic tumors (EHT). The 5-year cumulative incidence of IHT was 1.55% (95% CI 0.96–2.48) for IFN-based therapy, 4.27% (95% CI 2.93–6.2) for DAA and 0.89% (95% CI 0.4–1.99) for untreated patients. There was no statistically significant difference in the risk of developing IHT (HR = 1.34; 95% CI = [0.70; 2.58]; p = 0.380) or death (HR = 0.66; 95% CI = [0.43; 1.03]; p = 0.066) between patients treated with DAAs and those treated with IFN. Conclusions: The DAAs reduced the risk of death and were not associated with an increased risk of extrahepatic tumors (EHT). In the adjusted model, accounting for cirrhosis and high liver stiffness, the DAA treatment was associated with a higher risk of IHT occurrence compared with untreated patients, emphasizing the relevance of implementing standardized hepatocellular carcinoma (HCC) screening post-DAA treatment. Full article
(This article belongs to the Special Issue Hepatitis Viruses and Cancer)
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8 pages, 546 KiB  
Article
Hepatitis-C-Related Hepatocellular Carcinoma, Still a Relevant Etiology beyond a Hepatitis C Infection Cure
by Elena Vargas-Accarino, Mónica Higuera, María Buti and Beatriz Mínguez
Cancers 2024, 16(8), 1521; https://doi.org/10.3390/cancers16081521 - 16 Apr 2024
Cited by 1 | Viewed by 1459
Abstract
Background: In the past decades, global changes, including hepatitis B vaccination, hepatitis B and C antiviral therapies, and the increasing prevalence of steatotic liver disease, have influenced the landscape of liver cancer etiologies. Methods: We performed a retrospective study focused on the etiological [...] Read more.
Background: In the past decades, global changes, including hepatitis B vaccination, hepatitis B and C antiviral therapies, and the increasing prevalence of steatotic liver disease, have influenced the landscape of liver cancer etiologies. Methods: We performed a retrospective study focused on the etiological factors of de novo hepatocellular carcinoma (HCC) diagnoses in an academic center between 2019 and 2022. Results: Among 352 consecutive patients with HCC, alcohol-related liver disease was the predominant etiology (33.3%), followed by hepatitis C (HCV) infection (30.7%). Significant associations were found between HCC etiology and patient demographics, BCLC stage at diagnosis, and cirrhosis prevalence. Conclusions: Whereas accessibility to antiviral therapy is granted, HCV infection remains as one of the main HCC etiologies. MASLD-related HCC, although growing globally, is not as relevant in our area. Strong public policies need to be implemented to prevent alcohol consumption, the main etiology of liver disease and liver cancer. Full article
(This article belongs to the Special Issue Hepatitis Viruses and Cancer)
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