Hepatitis B virus infection and primary hepatocellular carcinoma

Feitelson, Mark A.

doi:10.1128/cmr.5.3.275

Cited by 71 publications

(25 citation statements)

References 342 publications

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“…Although the molecular mechanism by which HBV causes liver cancer is not well understood, the correlation between them is well established (Szmuness, 1979;Beasley et al, 1981;Feitelson, 1992;Robinson, 1994). Because HCC develops many years after infection, HBV appears not to be an acutely transforming virus and multiple stages may be required for HCC to develop.…”

Section: Introductionmentioning

confidence: 99%

Identification and characterization of a prevalent hepatitis B virus X protein mutant in Taiwanese patients with hepatocellular carcinoma

et al. 2000

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Section: Introductionmentioning

confidence: 99%

Identification and characterization of a prevalent hepatitis B virus X protein mutant in Taiwanese patients with hepatocellular carcinoma

et al. 2000

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“…Hepatocellular carcinoma (HCC) has been demonstrated to be strongly related to chronic hepatitis virus infection [1] and is a major cause of death among patients with cirrhosis (CIR) [2]. Especially in China, most of HCC patients have the disease background of chronic hepatitis B (CHB) or further CIR.…”

Section: Introductionmentioning

confidence: 99%

Serum metabolomics reveals the deregulation of fatty acids metabolism in hepatocellular carcinoma and chronic liver diseases

et al. 2012

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Patients with chronic liver diseases (CLD) including chronic hepatitis B and hepatic cirrhosis (CIR) are the major high-risk population of hepatocellular carcinoma (HCC). The differential diagnosis between CLD and HCC is a challenge. This work aims to study the related metabolic deregulations in HCC and CLD to promote the discovery of the differential metabolites for distinguishing the different liver diseases. Serum metabolic profiling analysis from patients with CLD and HCC was performed using a liquid chromatography-mass spectrometry system. The acquired large amount of metabolic information was processed with the random forest-recursive feature elimination method to discover important metabolic changes. It was found that long-chain acylcarnitines accumulated, whereas free carnitine, medium and short-chain acylcarnitines decreased with the severity of the non-malignant liver diseases, accompanied with corresponding alterations of enzyme activities. However, the general changing extent was smaller in HCC than in CIR, possibly due to the special energy-consumption mechanism of tumor cells. These observations may help to understand the mechanism of HCC occurrence and progression on the metabolic level and provide information for the identification of early and differential metabolic markers for HCC.

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“…Studies with regenerating mouse liver indicate that during late G 1 phase the nuclear levels of both subunits of DDB are transiently increased, followed by a sharp decrease in S phase. Taken together, these results suggest that DDB1 and DDB2 would participate in the nuclear functions of HBx effectively only during the late-G 1 phase of the cell cycle.Chronic infection with hepatitis B virus (HBV) is believed to be one of the key risk factors for the development of hepatocellular carcinoma (2,11,26,33,43). Despite the existence of successful vaccination programs, human HBV continues to be a major health problem, affecting around 350 million people worldwide (16).…”

mentioning

confidence: 99%

“…Chronic infection with hepatitis B virus (HBV) is believed to be one of the key risk factors for the development of hepatocellular carcinoma (2,11,26,33,43). Despite the existence of successful vaccination programs, human HBV continues to be a major health problem, affecting around 350 million people worldwide (16).…”

mentioning

confidence: 99%

DDB2 Induces Nuclear Accumulation of the Hepatitis B Virus X Protein Independently of Binding to DDB1

Nag

Datta²,

Yoo

et al. 2001

J Virol

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The hepatitis B virus (HBV) X protein (HBx) is critical for the life cycle of the virus. HBx associates with several host cell proteins including the DDB1 subunit of the damaged-DNA binding protein DDB. Recent studies on the X protein encoded by the woodchuck hepadnavirus have provided correlative evidence indicating that the interaction with DDB1 is important for establishment of infection by the virus. In addition, the interaction with DDB1 has been implicated in the nuclear localization of HBx. Because the DDB2 subunit of DDB is required for the nuclear accumulation of DDB1, we investigated the role of DDB2 in the nuclear accumulation of HBx. Here we show that expression of DDB2 increases the nuclear levels of HBx. Several C-terminal deletion mutants of DDB2 that fail to bind DDB1 are able to associate with HBx, suggesting that DDB2 may associate with HBx independently of binding to DDB1. We also show that DDB2 enhances the nuclear accumulation of HBx independently of binding to DDB1, since a mutant that does not bind DDB1 is able to enhance the nuclear accumulation of HBx. HBV infection is associated with liver pathogenesis. We show that the nuclear levels of DDB1 and DDB2 are tightly regulated in hepatocytes. Studies with regenerating mouse liver indicate that during late G 1 phase the nuclear levels of both subunits of DDB are transiently increased, followed by a sharp decrease in S phase. Taken together, these results suggest that DDB1 and DDB2 would participate in the nuclear functions of HBx effectively only during the late-G 1 phase of the cell cycle.Chronic infection with hepatitis B virus (HBV) is believed to be one of the key risk factors for the development of hepatocellular carcinoma (2,11,26,33,43). Despite the existence of successful vaccination programs, human HBV continues to be a major health problem, affecting around 350 million people worldwide (16). HBV belongs to the hepadnavirus family, which includes rodent viruses, such as woodchuck hepatitis virus (WHV) and ground squirrel hepatitis virus, and the distantly related duck hepatitis virus. The X gene of mammalian HBV encodes a small (17-kDa) multifunctional protein named HBx, which shares no similarity with any other known viral or cellular protein (25). HBx has been shown to affect a number of cellular processes (reviewed in reference 1). Among the best documented functions, transcriptional transactivation of several cellular and viral promoters (reviewed in references 7, 34, and 48) and stimulation of the apoptotic pathway (4,8,19,31,42) have received a wide range of experimental support. HBx has also been reported to inhibit the transactivation function and cause cytoplasmic sequestration of p53 (13,44,46).Previous studies have shown that HBx binds to the DDB1 subunit (125 kDa) of UV-damaged DNA binding protein (DDB) (3,20,40). DDB has been implicated in DNA repair (10,14,15,17,18,28,30,32,45). Mutational analysis of HBx has demonstrated a partial correlation between the reduction of repair activity in cells expressing HBx and the abi...

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Hepatitis B virus infection and primary hepatocellular carcinoma

Cited by 71 publications

References 342 publications

Identification and characterization of a prevalent hepatitis B virus X protein mutant in Taiwanese patients with hepatocellular carcinoma

Identification and characterization of a prevalent hepatitis B virus X protein mutant in Taiwanese patients with hepatocellular carcinoma

Serum metabolomics reveals the deregulation of fatty acids metabolism in hepatocellular carcinoma and chronic liver diseases

DDB2 Induces Nuclear Accumulation of the Hepatitis B Virus X Protein Independently of Binding to DDB1

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