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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 7, 2016; 22(1): 300-325
Published online Jan 7, 2016. doi: 10.3748/wjg.v22.i1.300
Published online Jan 7, 2016. doi: 10.3748/wjg.v22.i1.300
Hepatocellular carcinoma mouse models: Hepatitis B virus-associated hepatocarcinogenesis and haploinsufficient tumor suppressor genes
Yuan-Chi Teng, Ting-Fen Tsai, Program in Molecular Medicine, National Yang-Ming University, Taipei 112, Taiwan
Zhao-Qing Shen, Ting-Fen Tsai, Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan
Cheng-Heng Kao, Center of General Education, Chang Gung University, Taoyuan 333, Taiwan
Ting-Fen Tsai, Aging and Health Research Center, National Yang-Ming University, Taipei 112, Taiwan
Ting-Fen Tsai, Genome Research Center, National Yang-Ming University, Taipei 112, Taiwan
Ting-Fen Tsai, Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Miaoli 350, Taiwan
Author contributions: Teng YC, Shen ZQ and Kao CH contributed equally to this work; Teng YC drafted a portion of the manuscript and prepared Table 1; Shen ZQ drafted a portion of the manuscript and prepared Table 2 and Figure 2; Kao CH designed and prepared Figure 1; Tsai TF organized and wrote the final manuscript.
Supported by Research grants from the Ministry of Science and Technology (MOST) in Taiwan, No. NSC99-2628-B-010-001-MY3, MOST 103-2321-B-010-003, MOST 103-2633-H-010-001, MOST 103-2633-B-400-002 and MOST104-3011-B-010-001; and a grant from the Ministry of Education, Aim for the Top University Plan.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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/
Correspondence to: Ting-Fen Tsai, PhD, Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, 155 Li-Nong Street, Sec. 2, Beitou, Taipei 112, Taiwan. tftsai@ym.edu.tw
Telephone: +886-2-28267293 Fax: +886-2-28280872
Received: May 18, 2015
Peer-review started: May 20, 2015
First decision: September 9, 2015
Revised: October 14, 2015
Accepted: November 24, 2015
Article in press: November 24, 2015
Published online: January 7, 2016
Processing time: 226 Days and 17.8 Hours
Peer-review started: May 20, 2015
First decision: September 9, 2015
Revised: October 14, 2015
Accepted: November 24, 2015
Article in press: November 24, 2015
Published online: January 7, 2016
Processing time: 226 Days and 17.8 Hours
Core Tip
Core tip: Hepatitis B virus (HBV) viral products, in particular the oncogenic HBV X protein, and mutations of tumor suppressor genes (TSGs) are the driving force of hepatocellular carcinoma (HCC). Inactivation of a recessive TSG requires mutations in both alleles and fits the “two-hit” model. However, haploinsufficiency occurs when one allele is insufficient to confer the full functionality of a TSG; the gene’s effect can be partial or complete depending on tissue type, genetic modifiers/background, and environmental factors. Mouse models play a pivotal role in demonstrating the oncogenic effects of viral products and in establishing the dose-dependency and quantitative differences when analyzing a TSG involved in HCC.