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Liu et al. Hepatoma Res 2019;5:30 Hepatoma Research
DOI: 10.20517/2394-5079.2019.27

Editorial Open Access

The role of APOBEC3B in the development of
hepatocellular carcinoma should be investigated

with the consideration of hepatitis B virus evolution

Wen-Bin Liu, Guang-Wen Cao

Department of Epidemiology, Second Military Medical University, Shanghai 200433, China.
Correspondence to: Prof. Guang-Wen Cao, Department of Epidemiology, Second Military Medical University, 800 Xiangyin Rd,
Shanghai 200433, China. E-mail: gcao@smmu.edu.cn
How to cite this article: Liu WB, Cao GW. The role of APOBEC3B in the development of hepatocellular carcinoma should be
investigated with the consideration of hepatitis B virus evolution. Hepatoma Res 2019;5:30.
http://dx.doi.org/10.20517/2394-5079.2019.27

Received: 16 Jul 2019 First Decision: 17 Jul 2019 Revised: 17 Jul 2019 Accepted: 19 Jul 2019 Published: 7 Aug 2019
Science Editor: Guang-Wen Cao Copy Editor: Jia-Jia Meng Production Editor: Jing Yu

Received: First Decision: Revised: Accepted: Published: The chronic infection of hepatitis B virus (HBV) is the major cause of hepatocellular carcinoma (HCC)
[1]
globally . In Eastern China, chronic HBV infection contributes to 87.5% of HCC whereas chronic hepatitis
Science Editor: Copy Editor: Production Editor: Jing Yu
[2]
C virus (HCV) infection contributes to 1.7% . The mortality of HCC has increased in Europe and America
over recent decades . Although the infection of HCV is the leading cause of HCC in most European and
[3]
[3]
American countries, the contribution of HBV is increasing possibly due to immigration .
HCC represents a typical paradigm of inflammation-cancer transformation. Based on the advances in HBV-
induced hepatocarcinogenesis, a scientific theory of Cancer Evolution-Development (Cancer Evo-Dev) was
[4-6]
proposed . The central aspects of this theory include: the interaction of HBV infection and immunogenetic
predispositions maintains non-resolving inflammation. Immune imbalance promotes the generation
of somatic and viral mutations via disbalancing Apolipoprotein B mRNA-editing enzyme catalytic
polypeptide-like 3B (APOBEC3B) and mutation-repairing forces. Most mutant cells are eliminated by
inflammatory microenvironment while only a small percentage of cells adapt the environment and survive.
These survived mutant clones evolve to tumor-initiating cells (TICs) by altering the signal patterns mainly
caused by de-differentiation mechanisms. TICs acquire the stemness and the ability of immune escape
through recruiting tumor-associated macrophages (TAM) and myeloid-derived suppressor cells (MDSCs).
Under the pressure of selection, TICs further obtain metastatic and drug-resistant potentials to adapt to
distinct microenvironments. The evolution of HBV occurs along with this process. The mutant virus that
selected by inflammatory environment can survive the immune elimination and facilitate the malignant

© The Author(s) 2019. Open Access This article is licensed under a Creative Commons Attribution 4.0
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