Risk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levels

Yuen, Man‐Fung; Tanaka, Yasuhito; Shinkai, Noboru; Poon, Ronnie Tung‐Ping; But, David; Fong, Daniel Yee Tak; Fung, James; Wong, Danny Ka‐Ho; Yuen, Jason; Mizokami, Masashi; Lai, Ching–Lung

doi:10.1136/gut.2007.119859

Cited by 157 publications

(165 citation statements)

References 34 publications

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“…To our knowledge, the current case-control study is the first to reveal the association between HBV mutations and the development of HCC among Thai patients. In this study, we found that double A1762T/G1764A mutations were an independent risk factor for the development of HCC, which was consistent with recent casecontrol studies conducted in China, Taiwan, and Korea [7,12,20,21]. Also, the magnitude of the OR of HCC associated with the presence of the BCP double mutants in this study was approximately 3 to 4-fold, which was similar with reports of other studies.…”

Section: Discussionsupporting

confidence: 92%

“…These dual mutants have been reported in up to 50-80% of patients with HBeAg-negative chronic hepatitis B in Europe and Asia [6], and have been implicated in HCC development [7][8][9]. Apart from these variants, other mutations, such as T1753C/A/G in the BCP region and C1653T in the enhancer II region (EnhII) have become increasingly recognized as being associated with the outcome of chronic HBV infection, including HCC development [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

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A case–control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma

et al. 2010

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Purpose To evaluate the sequence variations in the enhancer II (EnhII)/basal core promotor (BCP)/precore (PC) and X genes of hepatitis B virus (HBV) in Thai patients with hepatocellular carcinoma (HCC) by conducting a cross-sectional case-control study. Methods As much as 60 patients with HCC and 60 patients without HCC, who were matched for sex, age, hepatitis B e antigen (HBeAg) status, and HBV genotype, were included. Viral mutations in the EnhII/BCP/PC and X regions were characterized by direct sequencing in serum samples.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

A case–control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma

et al. 2010

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“…In fact, several studies reported that genotype C was related to a higher risk of HCC development as compared to genotype B, although such association was not confirmed by other studies (Kim et al, 2011). Additionally, we found significantly higher frequencies of A1762T/G1764A and T1753A/G/C mutations in the HCC group than in controls, which are consistent with previous reports (Chen et al, 2008;Yuen et al, 2008). In fact, T1753A/G/C mutations are usually present along with the existence of A1762T/ G1764A mutations.…”

Section: Discussionsupporting

confidence: 67%

Hepatitis B Virus Genetic Variation and TP53 R249S Mutation in Patients with Hepatocellular Carcinoma in Thailand

Thongbai

Sa-nguanmoo²,

Kranokpiruk³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Chronic hepatitis B virus (HBV) infection and dietary exposure to aflatoxin B1 (AFB1) are major risk factors for hepatocellular carcinoma (HCC). The aim of this study was to evaluate the role of HBV genetic variation and the R249S mutation of the p53 gene, a marker of AFB1-induced HCC, in Thai patients chronically infected with HBV. Sixty-five patients with and 89 patients without HCC were included. Viral mutations and R249S mutation were characterized by direct sequencing and restriction fragment length polymorphism (RFLP) in serum samples, respectively. The prevalences of T1753C/A/G and A1762T/G1764A mutations in the basal core promotor (BCP) region were significantly higher in the HCC group compared to the non-HCC group. R249S mutation was detected in 6.2% and 3.4% of the HCC and non-HCC groups, respectively, which was not significantly different. By multiple logistic regression analysis, the presence of A1762T/G1764A mutations was independently associated with the risk of HCC in Thai patients.

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“…Similarly, Yuen et al from Hong Kong examined the risks for HCC with respect to HBV genotypes, specific viral mutants, serum HBV DNA levels, and cirrhosis in a case-control study, and multivariate analysis showed that core promoter mutant, T1653, HBV DNA ‡2,000 IU/ml, and cirrhosis were independent factors for HCC. In addition, the risks remarkably increased in HBV carriers with these factors in combination [90]. In Japan, an age-, sex-, and HBeAg status-matched cross-sectional control study was conducted to determine HCC-associated mutations of the HBV genome in the entire X, core promoter, and precore/core regions among 80 patients infected with HBV subgenotype C2 with HCC and 80 without HCC.…”

Section: Potential Interactions Between Known Hbv Factorsmentioning

confidence: 99%

Role of viral factors in the natural course and therapy of chronic hepatitis B

Kao

2007

Hepatol Int

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Hepatitis B virus (HBV) infection is a global health problem that causes a wide spectrum of liver disease, including acute or fulminant hepatitis, inactive carrier state, chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). The pathogenesis of hepatocyte damage associated with HBV is mainly through immune-mediated mechanisms. On the basis of the virus and host interactions, the natural history of HBV carriers who are infected in early life can be divided into four dynamic phases. The frequency, extent, and severity of hepatitis flares or acute exacerbation in the second immune clearance and/or fourth reactivation phase predict liver disease progression in HBV carriers. In the past decade, hepatitis B viral factors including serum HBV DNA level, genotype, and naturally occurring mutants predictive of clinical outcomes have been identified. The higher the serum HBV DNA level after the immune clearance phase, the higher the incidence of adverse outcomes over time. In addition, high viral load, genotype C, basal core promoter mutation, and pre-S deletion correlate with increased risk of cirrhosis and HCC development. As to the treatment of chronic hepatitis B, patients with high HBV DNA level and genotype C or D infection are shown to have a worse response to interferon therapy. In conclusion, serum HBV DNA level, genotype, and naturally occurring mutants are identified to influence liver disease progression and therapy of chronic hepatitis B. More investigations are needed to clarify the molecular mechanisms of the viral factors involved in the pathogenesis of each stage of liver disease and the response to antiviral treatments.

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Risk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levels

Abstract: CP-MT, T1653, HBV DNA levels >or=4 log(10) copies/ml and cirrhosis are independent factors for development of HCC. The risks increased substantially in patients having these factors in combination.

Cited by 157 publications

References 34 publications

A case–control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma

A case–control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma

Hepatitis B Virus Genetic Variation and TP53 R249S Mutation in Patients with Hepatocellular Carcinoma in Thailand

Role of viral factors in the natural course and therapy of chronic hepatitis B

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