Impact of non-neoplastic vs intratumoural hepatitis B viral DNA and replication on hepatocellular carcinoma recurrence.
Impact of non-neoplastic vs intratumoural hepatitis B viral DNA and replication on hepatocellular carcinoma recurrence.
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DOI：
10.1038/bjc.2016.239
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发表时间：
2016-09-27
影响因子：
8.8
通讯作者：
Hiotis, Spiros P.
中科院分区：
文献类型：
--
作者：
Wang, Qin;Lin, Luan;Yoo, Seungyeul;Wang, Wenhui;Blank, Sima;Fiel, M. Isabel;Kadri, Hena;Luan, Wei;Warren, Leslie;Zhu, Jun;Hiotis, Spiros P.
This study aims to determine the impact of intracellular hepatitis B virus (HBV) DNA, covalently closed circular DNA (cccDNA) and viral replicative activity in both tumour and non-neoplastic liver on prognosis and to determine the relationship of viral replicative activity and Ishak fibrosis in predicting outcome following resection. A total of 99 prospectively enrolled patients treated with primary liver resection for HBV-HCC are included. Intracellular HBV DNA and cccDNA were quantitated by real-time PCR. The RNA-sequencing (RNA-seq) was performed in a subset of 21 patients who had either minimal liver fibrosis (Ishak stages 0–2) or end-stage fibrosis (Ishak stage 6). Tumour tissue contained a lower cccDNA copy number compared with paired non-neoplastic liver, and larger tumours (>3 cm) had less cccDNA compared with small tumours (⩽3 cm). High viral replicative activity in non-neoplastic liver was associated with higher HCC recurrence rate independent of Ishak fibrosis stage. Genes correlated with viral replicative activity in non-neoplastic liver (620 genes) were distinct from those associated with end-stage fibrosis (1226 genes). Genes associated with viral replicative activity were preferentially distributed in regions on chr3, chr16 and chr19. Viral replicative activity in non-neoplastic liver is associated with HCC recurrence through mechanisms that are distinct from and independent of Ishak fibrosis stage.
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影响因子：
13.5
作者：
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通讯作者：
Dandri, Maura
影响因子：
29.4
作者：
Volz, Tassilo;Lutgehetmann, Marc;Petersen, Joerg
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Szczyrba, Jaroslaw;Nolte, Elke;Graesser, Friedrich A.
通讯作者：
Graesser, Friedrich A.
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29.4
作者：
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Samuel, Didier