Hepatocellular carcinoma mouse models: Hepatitis B virusassociated hepatocarcinogenesis and haploinsufficient tumor suppressor genes

Yuan Chi Teng, Zhao Qing Shen, Cheng Heng Kao, Ting Fen Tsai*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

The multifactorial and multistage pathogenesis of hepatocellular carcinoma (HCC) has fascinated a wide spectrum of scientists for decades. While a number of major risk factors have been identified, their mechanistic roles in hepatocarcinogenesis still need to be elucidated. Many tumor suppressor genes (TSGs) have been identified as being involved in HCC. These TSGs can be classified into two groups depending on the situation with respect to allelic mutation/loss in the tumors: the recessive TSGs with two required mutated alleles and the haploinsufficient TSGs with one required mutated allele. Hepatitis B virus (HBV) is one of the most important risk factors associated with HCC. Although mice cannot be infected with HBV due to the narrow host range of HBV and the lack of a proper receptor, one advantage of mouse models for HBV/HCC research is the numerous and powerful genetic tools that help investigate the phenotypic effects of viral proteins and allow the dissection of the dose-dependent action of TSGs. Here, we mainly focus on the application of mouse models in relation to HBV-associated HCC and on TSGs that act either in a recessive or in a haploinsufficient manner. Discoveries obtained using mouse models will have a great impact on HCC translational medicine.

Original languageEnglish
Pages (from-to)300-325
Number of pages26
JournalWorld Journal of Gastroenterology
Volume22
Issue number1
DOIs
StatePublished - 7 Jan 2016

Keywords

  • Haploinsufficiency
  • Hepatitis B virus
  • Hepatocellular carcinoma
  • Mouse models
  • Tumor suppressor genes

Fingerprint

Dive into the research topics of 'Hepatocellular carcinoma mouse models: Hepatitis B virusassociated hepatocarcinogenesis and haploinsufficient tumor suppressor genes'. Together they form a unique fingerprint.

Cite this