Independent risk factors and predictive score for the development of hepatocellular carcinoma in chronic hepatitis B

Yuen, Man‐Fung; Tanaka, Yasuhito; Fong, Daniel Yee Tak; Fung, James; Wong, Danny Ka‐Ho; Yuen, Jason; But, David; Chan, Annie On‐On; Wong, Benjamin Chun–Yu; Mizokami, Masashi; Lai, Ching–Lung

doi:10.1016/j.jhep.2008.07.023

Cited by 537 publications

(555 citation statements)

References 32 publications

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“…Epidemiologic cohort studies have demonstrated that male gender, increasing age, cirrhosis, high viral load (!10 4 copies/ml), hepatitis B e antigen (HBeAg) expression, HBV genotype C2 (vs. genotype B2), low albumin, and elevated alanine aminotransferase (ALT) increase the risk of HCC in chronic HBV-infected patients (11)(12)(13)(14)(15). Some of these risk factors have been used to construct clinical scoring systems for the prediction of HCC (12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Yin

Wang

et al. 2015

Cancer Prevention Research

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We aimed to evaluate whether hepatitis B virus (HBV) mutations at the core promoter region could improve the prediction and specific prophylaxis of hepatocellular carcinoma (HCC) in chronic HBV-infected patients. A total of 2,114 HBV-infected patients enrolled between August 1998 and December 2007 were followed-up for 18,406 person-years. Of those, 612 received !48 week treatments with nucleos(t)ide analogue (NA) and/or IFNa.

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Section: Introductionmentioning

confidence: 99%

Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Yin

Wang

et al. 2015

Cancer Prevention Research

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“…(2) Substantial evidence from epidemiological studies indicates that HCC is strongly associated with alcohol abuse, chronic infection with hepatitis B virus (HBV) and/or hepatitis C virus (HCV), and liver cirrhosis. (3)(4)(5) More than one million people die of liver cancer worldwide every year. (6) Few patients are diagnosed in the early stage, and <20% of HCCs can be resected completely.…”

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confidence: 99%

MARVELD1 inhibited cell proliferation and enhance chemosensitivity via increasing expression of p53 and p16 in hepatocellular carcinoma

Zhang

et al. 2012

Cancer Science

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We have previously found that expression of MARVELD1 was remarkably downregulated in multiple tumor tissues, but unclear in hepatocellular carcinoma (HCC) and its function has not been explored yet. In the present study, to uncover the underlying mechanism of MARVELD1 in the pathogenesis and development of HCC, we investigated the expression pattern of MARVELD1 and its effect on tumor proliferation in HCC. The results indicated the frequent downregulation of MARVELD1 in clinic samples and cell lines of HCC resulted from promoter methylation, as well as genetic deletion. Furthermore, treatment of MARVELD1 unexpressing Hep3B2.1-7 and PLC/PRF/5 cells with the demethylating agent 5-aza-2′ deoxycytidine restored its expression. Overexpression of MARVELD1 suppressed the proliferation of HCC cells in vitro and in vivo, whereas downregulation of endogenous MARVELD1 by shRNAs significantly enhanced these characters. MARVELD1 overexpression could enhance chemosensitivity of HCC cells to epirubicin and 10-hydroxycamptothecin. Corresponding to these results, the expression of p-ERK1/2 and cyclin D1 were decreased, whereas p16 and p53 were increased in MAR-VELD1-transfected cells. We also demonstrated that knockdown of MARVELD1 resulted in upregulation of p-ERK1/2 and cyclin D1, and downregulation of p16 and p53. Moreover, the effect of the decreased cell growth rate was significantly reversed when MAR-VELD1-overexpressing cells were trasfected with p53 or p16 siR-NA. Our findings suggest that MARVELD1 is a tumor suppressor by negatively regulating proliferation, tumor growth and chemosensitivity of HCC cells via increasing p53 and p16 in vitro and in vivo. MARVELD1 may be a potential target for HCC therapy. (Cancer Sci 2012; 103: 716-722) H epatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide, and its incidence is still rising.(1) Currently there are about 600 000 cases of HCC each year, and nearly 78% of them are from Asian countries.(2) Substantial evidence from epidemiological studies indicates that HCC is strongly associated with alcohol abuse, chronic infection with hepatitis B virus (HBV) and/or hepatitis C virus (HCV), and liver cirrhosis.(3-5) More than one million people die of liver cancer worldwide every year.(6) Few patients are diagnosed in the early stage, and <20% of HCCs can be resected completely. (7,8) Resistance to many of chemotherapy agents is a major obstacle to successful HCC treatment.(9-11) Therefore, a better understanding of the molecular mechanisms underlying HCC progression is urgently needed for leading to a more effective treatment.Genetic and epigenetic aberrations, leading to the activation of oncogenes and inactivation of tumor suppressor genes, are thought to play major roles in the pathogenesis of HCC. Recently, several MARVEL (proteins of the myelin and lymphocytes [MAL] and related proteins for vesicle trafficking and membrane link) domain-containing proteins have attracted increasing interest because they exhibit tumor suppressor activities a...

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“…A pattern is outlined in which pockets of chronic HBV carriers are identified where potential reservoirs are concentrated. The importance of vertical transmission in the region has also been determined, and is probably one of the mechanisms responsible for maintaining HBV circulation in populations at high risk of developing liver cirrhosis and hepatocellular carcinoma 59 caused by the burden of HDV infection. The continued expansion of migrations of individuals from HBV endemic areas has a significant impact on the epidemiology and increased prevalence of chronic hepatitis B in areas previously considered non-endemic.…”

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confidence: 99%

Epidemiology and Molecular Characterization of Hepatitis B Virus Infection in Isolated Villages in the Western Brazilian Amazon

Castilho

Oliveira

Gimaque

et al. 2012

The American Society of Tropical Medicine and Hygiene

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Abstract. Individuals from three isolated, rural communities in the western Brazilian Amazon were evaluated for serological markers of hepatitis B virus (HBV) infection, HBV genotype, and the presence of risk factors for infection and transmission. Of the 225 individuals studied, 79.1% had serological evidence of HBV infection; 10.2% individuals were chronic carriers for HBV surface antigen (HBsAg-positive). Analysis of risk factors indicates that HBV is transmitted mainly horizontally within the family from a chronic "active" carrier for hepatitis B "e" antigen (HBeAgpositive), though a strong possibility of vertical transmission remains. The predominance of HBV genotype F, with a higher genomic similarity between the isolates, indicated a relatively recent introduction of HBV, from a common source, to the area. This study sheds light on the HBV epidemiology in the Brazilian Amazon region and highlights the need for greater emphasis on HBV control and immunization programs.

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Independent risk factors and predictive score for the development of hepatocellular carcinoma in chronic hepatitis B

Cited by 537 publications

References 32 publications

Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

MARVELD1 inhibited cell proliferation and enhance chemosensitivity via increasing expression of p53 and p16 in hepatocellular carcinoma

Epidemiology and Molecular Characterization of Hepatitis B Virus Infection in Isolated Villages in the Western Brazilian Amazon

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