Review
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Jul 6, 2021; 9(19): 4890-4917
Published online Jul 6, 2021. doi: 10.12998/wjcc.v9.i19.4890
Molecular pathways in viral hepatitis-associated liver carcinogenesis: An update
Gulsum Ozlem Elpek
Gulsum Ozlem Elpek, Department of Pathology, Akdeniz University Medical School, Antalya 07070, Turkey
Author contributions: GO Elpek performed the design of the article, obtained, analyzed, and interpreted the data, and wrote the article.
Conflict-of-interest statement: No conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Gulsum Ozlem Elpek, MD, Professor, Department of Pathology, Akdeniz University Medical School, Dumlupınar Bulvarı, Antalya 07070, Turkey. elpek@akdeniz.edu.tr
Received: January 23, 2021
Peer-review started: January 23, 2021
First decision: February 28, 2021
Revised: March 14, 2021
Accepted: May 26, 2021
Article in press: May 26, 2021
Published online: July 6, 2021
Processing time: 151 Days and 18.3 Hours
Core Tip

Core Tip: Hepatocellular carcinoma remains an aggressive tumor, despite extensive studies on its ontogeny and prognosis. Although the occurrence of this tumor in both hepatitis B virus (HBV) and hepatitis C virus (HCV) backgrounds indicates the effect of persistent inflammation in malignant transformation, the viral effects are not limited to the impaired microenvironment. Recent studies have revealed complex mechanisms that reflect concerted and cumulative effects of chronic inflammation-related alterations, modification of oncogenic pathways (especially tumor suppression, proliferation, and apoptosis), and epigenetic dysregulation driven by both HBV and HCV. In addition, the integration of HBV into host DNA may also affect tumor development and behavior.