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Rate of Persistence, Structure, and Expression of HBV Genome in HCC Developing in HBsAg-negative Patients

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TLDR
Results suggest a role for the potentially transforming, transactivating X protein in the HBV-related liver carcinogenesis in HBsAg-negative patients.
Abstract
HBV genomes have been described even in HBsAg-negative patients with hepatocellular carcinoma (HCC), but the role of hepatitis B virus (HBV) in liver transformation is still unclear. We assessed the rate of persistence, the structure, and the RNA expression of HBV genomes in HBsAg-negative HCC using HBV- DNA PCR and HBV-RNA RT-PCR. HBV DNA genomes have been detected in 37 (59%) of 63 HBsAg-negative HCC. Defective genomes have been found more frequently in tumorous than nontumorous tissues (19/29 vs 1/9) and in seronegative than seroconverted patients (9/12 vs 1/7). A significant accumulation of X RNA was shown in 7/9 tumorous and 7/8 nontumorous tissues. By contrast, S and C RNAs were barely expressed in both tumorous and nontumorous tissues. These results suggest a role for the potentially transforming, transactivating X protein in the HBV-related liver carcinogenesis in HBsAg-negative patients.

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HCV-associated liver cancer without cirrhosis

TL;DR: The results provide evidence for the association of HCV, mostly genotype 1b, with hepatocellular cancer without the intermediate step of cirrhosis.
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Pathogenesis of hepatitis B and C-induced hepatocellular carcinoma

TL;DR: It is probable that the ongoing process of hepatocyte necrosis and liver cell renewal coupled with inflammation, which is characteristic of chronic viral hepatitis, causes not only nodular regeneration and cirrhosis but also progressive genomic errors in hepatocytes as well as unregulated growth and repair mechanisms leading to hepatocyte dysplasia and, in some cases, hepatic carcinoma.
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Occult hepatitis B virus and hepatitis C virus infections.

TL;DR: Occult HBV infection in patients with chronic HCV infection may induce more severe liver disease and lower response rate to interferon treatment and the clinical relevance of occult HCV infections is still under investigation.
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Hepatitis C virus: molecular biology and genetic variability.

TL;DR: The pathogenetic mechanisms of hepatitis C virus (HCV) infection are poorly known, and there is evidence for a potential direct effect of HCV in liver carcinogenesis, with subtype 1b possibly being an independent risk factor for hepatic carcinoma development.
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Association between chronic hepatitis C infection and hepatocellular carcinoma in a Scottish population.

TL;DR: There is a strong association between chronic HCV infection, cirrhosis, and hepatocarcinogenesis in this Scottish population of patients presenting to a single hospital.
References
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Journal ArticleDOI

Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction

TL;DR: A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described, providing a pure preparation of undegraded RNA in high yield and can be completed within 4 h.
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HBx gene of hepatitis B virus induces liver cancer in transgenic mice

TL;DR: This transgenic animal model appears ideal for defining the molecular events that follow the expression of the viral HBx gene and are responsible for the development of liver cancer.
Journal ArticleDOI

Hepatitis B virus integration in a cyclin A gene in a hepatocellular carcinoma.

TL;DR: The cloning of a single HBV integration site in a human hepatocellular carcinoma at an early stage of development is reported, and of its germline counterpart is reported.
Journal ArticleDOI

Hepatitis b virus dna in patients with chronic liver disease and negative tests for hepatitis b surface antigen

TL;DR: This study demonstrates the high frequency of HBsAg-negative HBV DNA-positive viral infection of the liver and suggests that multiplication of HBV may occur in the absence of any conventional serologic marker for HBV.
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