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Review : Molecular Pathogenesis of Hepatitis-B-virus-associated Hepatocellular Carcinoma
( Neung Hwa Park ),( Il Han Song ),( Young Hwa Chung ) The Editorial Office of Gut and Liver 2007 Gut and Liver Vol.1 No.2
Hepatocellular carcinoma (HCC) is one of the most frequent and malignant diseases worldwide. Epidemiological studies have clearly demonstrated that chronic hepatitis B virus (HBV) infection is a major etiological factor in the development of HCC. The pathogenesis of HBV-associated HCC has been studied extensively, and the molecular changes associated with malignant transformation have been identified. The predominant carcinogenic mechanisms of HBV-associated HCC are chronic inflammation and the effects of cytokines in the development of fibrosis and liver cell proliferation. An important role is also played by the integration of HBV DNA into host cellular DNA, which disrupts or promotes the expression of cellular genes that are important in cell growth and differentiation. Especially, HBx protein is a transactivating protein that promotes cell growth, survival, and the development of HCC. Continued investigation of the mechanisms underlying hepatocarcinogenesis will refine our current understanding of the molecular and cellular basis for neoplastic transformation in the liver. Prevention of HBV infections and effective treatments for chronic hepatitis B are still needed for the global control of HBV-associated HCC. This review summarizes the current knowledge on the mechanisms involved in HBV-associated hepatocarcinogenesis. (Gut and Liver 2007;1:101-117)
Inactivating Mechanism of ATBF1 Gene in Hepatocellular Carcinomas
( Neung Hwa Park ),( Chang Jae Kim ),( Jung Woo Shin ),( Seok Won Jung ),( Bo Ryung Park ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: Alpha-fetoprotein (AFP) is frequently detected in hepatocellular carcinomas (HCCs) and AT motif binding factor 1 (ATBF1) down-regulates AFP gene expression in hepatic cells. The ATBF1 gene also inhibits cell growth and differentiation and altered gene expression is associated with malignant transformation. Methods: To investigate the potential role of the ATBF1 gene in HCCs, we analyzed somatic mutations, allelic loss and hypermethylation of the ATBF1 gene in 45 sporadic HCCs. The level of ATBF-1 mRNA expression was analyzed using quantitative real-time RT-PCR. Results: Genetic studies of the ATBF1 gene revealed absence of a somatic mutation in the hotspot region and 5 (16.7%) of 30 informative cases showed allelic loss at the ATBF1 locus. Hypermethylation in the intron 1 region of the ATBF1 gene was detected in only one case. Interestingly, ATBF1 mRNA expression in HCCs was significantly reduced in 33 (73.3%) samples compared to the corresponding surrounding liver tissues. Conclusions: These results suggest that the ATBF1 gene may contribute to the development of HCCs via transcriptional down-regulation of mRNA expression, but not by genetic or epigenetic alterations.
Genetic Alterations of the SIAH-1 Gene in Hepatocellular Carcinomas
( Neung Hwa Park ),( Chang Jae Kim ),( Jung Woo Shin ),( Seok Won Jung ),( Bo Ryung Park ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: Siah-1 is the mammalian homolog of Drosophila seven in absentia (sina) and has been identified as a p53-inducible gene. Siah-1 can induce cell cycle arrests, tumor suppression, and apoptosis through a novel β-catenin degradation pathway. Methods: To determine whether genetic alterations of Siah-1 gene are involved in the development and/or progression of HCCs, we searched for mutation of the Siah-1 gene in 38 HCCs by single strand conformational polymorphism and sequencing. The effect of Siah-1 on β-catenin degradation was further examined in wild- and mutant- type Siah-1 transfected HEK 293T cells. Results: We found two frameshift mutations and one missense mutation of the Siah-1 gene. The cases with Siah-1 mutation showed nuclear translocation and cytoplasmic staining of β-catenin. Interestingly, three mutants of Siah-1 stabilized cytoplasmic levels of β -catenin, even after treatment of adriamycin. Furthermore, Three mutants failed to suppress cyclin D1 expression and to induce apoptosis. Conclusions: These data suggest that inactivating mutations of the Siah-1 may contribute to the development of HCCs through β-catenin stabilization and apoptosis block.
Impacts of Vaccination on Hepatitis B Viral Infections in Korea over a 25-Year Period
Park, Neung Hwa,Chung, Young-Hwa,Lee, Hyo-Suk S. Karger AG 2010 Intervirology Vol.53 No.1
<P><I>Background:</I> Hepatitis B virus (HBV) vaccination has effectively reduced the acute and chronic infection rates in recent years. Since 1983, HBV vaccination has been recommended for all neonates in Korea. <I>Methods:</I> This article reviews the impacts of HBV vaccination throughout the past 25 years in Korea. Before the introduction of the HBV vaccination program, approximately 8% of the general Korean population tested positive for hepatitis B virus surface antigen (HBsAg). <I>Results:</I> The percentage of vaccinated infants has surpassed 98.9% since 1990. The HBsAg carrier rate in the general population decreased to 3.7% in 2007. In particular, the prevalence of HBsAg decreased to 0.44% in teenagers and to 0.2% in children younger than 10 years. In addition, administration of the HBV vaccine may have reduced the risk of hepatocellular carcinoma among adults. Despite the administration of hepatitis B immunoglobulin and the HBV vaccine to children with HBsAg-positive mothers, the failure rate of HBV immunoprophylaxis was 4.2% in 2008. In Korea, there have been no reported cases of HBV surface gene variants such as G145R. <I>Conclusions:</I> The prevalence of HBV carriers in Korea was markedly reduced after the introduction of the universal HBV vaccination program. Korea is now classified as an area of intermediate endemicity for HBV.</P><P>Copyright © 2010 S. Karger AG, Basel</P>