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Fu et al. Hepatoma Res 2018;4:39                                 Hepatoma Research
               DOI: 10.20517/2394-5079.2018.29


               Review                                                                        Open Access


               Oxidative stress and hepatocarcinogenesis

                      1
               Ying Fu , Fung-Lung Chung 2
               1 Laboratory of Molecular Biology, Center for Cancer Research, NCI, Bethesda, MD 20892, USA.
               2 Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20007, USA.

               Correspondence to: Dr. Ying Fu, Laboratory of Molecular Biology, Center for Cancer Research, NCI, Bethesda, MD 20892, USA. E-mail:
               ying.fu@nih.gov; Dr. Fung-Lung Chung, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20007, USA.
               E-mail: flc6@georgetown.edu
               How to cite this article: Fu Y, Chung FL. Oxidative stress and hepatocarcinogenesis. Hepatoma Res 2018;4:39.
               http://dx.doi.org/10.20517/2394-5079.2018.29
               Received: 24 Mar 2018    First Decision: 5 Jul 2018    Revised: 12 Jul 2018    Accepted: 13 Jul 2018    Published: 1 Aug 2018

               Science Editor: Guang-Wen Cao    Copy Editor: Jun-Yao Li    Production Editor: Huan-Liang Wu


               Abstract
               Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. There are two
               major challenges for HCC, the first being that early detection is generally not applicable, and secondly, it is usually
               fatal within several months after diagnosis. HCC is an inflammation-induced cancer. It is known that chronic
               inflammation leads to oxidative/nitrosative stress and lipid peroxidation, generating excess oxidative stress,
               together with aldehydes which can react with DNA bases to form promutagenic DNA adducts. In this review, the
               evidence between oxidative stress and liver carcinogenesis is summarized. We focused on the potential of using
               DNA adducts as oxidative stress biomarkers for liver carcinogenesis.

               Keywords: Oxidative stress, DNA adduct, hepatocellular carcinoma, prevention, hepatocarcinogenesis





               INTRODUCTION
               Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide, because
                                                       [1-4]
               of late diagnosis and poor therapeutic outcome . HCC accounts for 5.5% of all cancer cases globally, and
                                                                                    [5,6]
               particularly the incidence of HCC has been increasing in the US since the 1980s . The incidence of HCC
               strongly correlates with liver inflammation from exposure to one or several risk factors including hepatitis B
               virus (HBV), hepatitis C virus (HCV), inherited metabolic diseases, heavy alcohol exposure, obesity, type 2
               diabetes and aflatoxins [7-13] .

               In this review, we will mainly discuss the role of oxidative stress in hepatocarcinogenesis. The search for
               reliable biomarkers for liver cancer has been executed in different areas: DNA methylation, genomics, pro-


                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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