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Liu et al. Hepatoma Res 2019;5:30 I http://dx.doi.org/10.20517/2394-5079.2019.27 Page 3 of 4
of APOBEC3-signature HBV mutations and A1762T/G1764A in HBV-infected subjects, both of which
were confirmed to associated with increased risk of HCC. The data of cohort studies demonstrated that
APOBEC3B rs2267401-GG genotype, higher APOBEC3B expression, and higher APOBEC3B/UNG
expression ratio in HCCs can predict a poor prognosis. Interestingly, APOBEC-signature somatic mutation
predicts poor prognosis only in HBV-free HCC rather than in HBV-positive ones. These evidences strongly
suggest that APOBEC3B facilitates HBV-induced HCC evolution via its mutagenic effect preferentially
on the HBV genome. This result also explains why the APOBEC3-signature somatic mutation was not
[11]
dominant in HCC genome . APOBEC3B prefers to edit HBV genome possibly because the number of
HBV genomic DNA is overwhelmingly more than that of human genome. Besides, during the replication
of HBV, the partially double-stranded HBV DNA is generated from an intermediate RNA that is vulnerable
to APOBEC3B.
To conclude, the work by Wang and related studies demonstrated the important role of APOBEC3B in
HCC evolution from different aspects. APOBEC3B promotes HBV-induced carcinogenesis through its
mutagenic activity and facilitating immune escape of HCC through regulating epigenetic modification.
The investigation for APOBEC3B can be transformed not only into specific prophylaxis but also into target
therapy.
DECLARATIONS
Authors’ contributions
Study concept and design: Cao GW
Drafting of the manuscript: Liu WB
Discussion and revision of the manuscript text: Cao GW
Availability of Data and Materials
Not applicable.
Financial support and sponsorship
This work was supported by grant (2015CB554006) from the National Key Basic Research Program of
China (GC).
Conflicts of interest
All authors declared that there are no conflicts of interest.
Ethical Approval and Consent to Participate
Not applicable.
Consent for publication
Not applicable.
Copyright
© The Author(s) 2019.
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