Clinical and Molecular Hepatology

"Nucleotide"

Letter to the Editor

Comment on the expert consensus on treatment approaches for achieving functional cure in chronic hepatitis B: Letter to the editor on “Update on the treatment navigation for functional cure of chronic hepatitis B: Expert consensus 2.0”: Seng-Gee Lim, Melanie Paff; Clin Mol Hepatol 2026;32(3):e285-e287.
Published online December 26, 2025; DOI: https://doi.org/10.3350/cmh.2025.1441

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Correspondence to letter to the editor on “Update on the treatment navigation for functional cure of chronic hepatitis B: Expert consensus 2.0”
Di Wu, Xiaojing Wang, Weiming Yan, Man-Fung Yuen, Qin Ning
Clinical and Molecular Hepatology.2026; 32(3): e408. CrossRef

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Original Article

Autoimmune liver disease

Safety and efficacy of HK-660S in patients with primary sclerosing cholangitis: A randomized double-blind phase 2a trial: Woo Hyun Paik, Joo Kyung Park, Moon Jae Chung, Gunn Huh, Ce Hwan Park, Sang Hyub Lee, Heon Se Jeong, Hee Jin Kim, Do Hyun Park; Clin Mol Hepatol 2025;31(1):119-130.
Published online September 24, 2024; DOI: https://doi.org/10.3350/cmh.2024.0629

Background/Aims
A clinical unmet need persists for medications capable of modulating the progression of primary sclerosing cholangitis (PSC). This study aimed to assess the clinical feasibility of HK-660S (beta-lapachone) in PSC.
Methods
In this multicenter, randomized, double-blind, placebo-controlled, parallel-group phase 2 trial, participants were assigned in a 2:1 ratio to receive either 100 mg of HK-660S or a placebo twice daily for 12 weeks. The primary outcomes were the reduction in serum alkaline phosphatase (ALP) levels and the percentage of participants showing improvements in PSC severity, as determined by magnetic resonance cholangiopancreatography with the Anali score. Secondary endpoints included changes in liver stiffness and adverse events.
Results
The analysis included 21 patients, 15 receiving HK-660S, and six receiving a placebo. Improvements in the Anali score were observed in 13.3% of the HK-660S group, with no improvements in the placebo group. HK-660S treatment resulted in a 15.2% reduction in mean ALP levels, compared to a 6.6% reduction in the placebo group. A stratified ad-hoc analysis based on baseline ALP levels showed a statistically significant response in the HK-660S group among those with ALP levels greater than twice the upper limit of normal, with a 50% responder rate (p=0.05). Additionally, 26.7% of the HK-660S group showed improvements in the enhanced liver fibrosis score, with no improvements in the placebo group. HK-660S was generally well tolerated.
Conclusions
HK-660S is well tolerated among patients with PSC and may improve bile duct strictures, decrease serum ALP levels, and reduce liver fibrosis (cris.nih.go.kr, Number KCT0006590).

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Critical considerations in evaluating the therapeutic potential of HK-660S for primary sclerosing cholangitis: Letter to the editor on “Safety and efficacy of HK-660S in patients with primary sclerosing cholangitis: a randomized double-blind phase 2a tria
Yizi He, Haifeng He, Qi Liang, Yongzhi Xie
Clinical and Molecular Hepatology.2026; 32(1): e1. CrossRef
Primary sclerosing cholangitis
Erik von Seth, Tom H Karlsen, Atsushi Tanaka, Cyriel Ponsioen, Annika Bergquist
The Lancet.2026; 407(10538): 1549. CrossRef
Pruritus in Chronic Cholestatic Liver Diseases, Especially in Primary Biliary Cholangitis: A Narrative Review
Tatsuo Kanda, Reina Sasaki-Tanaka, Naruhiro Kimura, Hiroyuki Abe, Tomoaki Yoshida, Kazunao Hayashi, Akira Sakamaki, Takeshi Yokoo, Hiroteru Kamimura, Atsunori Tsuchiya, Kenya Kamimura, Shuji Terai
International Journal of Molecular Sciences.2025; 26(5): 1883. CrossRef
Future Treatment Options for Managing Primary Sclerosing Cholangitis and Cholestatic Pruritus
Taranika Sarkar Das, Raj Vuppalanchi
Clinics in Liver Disease.2025; 29(4): 781. CrossRef

11,526 View
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Correspondence

Hepatic neoplasm

Correspondence to editorial on “KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression”: Sang Bae Lee, KyeongJin Kim; Clin Mol Hepatol 2025;31(1):e78-e80.
Published online September 10, 2024; DOI: https://doi.org/10.3350/cmh.2024.0750

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Multifaceted roles of KCTD17 in cellular homeostasis and disease
Yelin Jeong, HyunJoon Gi, Young Hoon Jung, Ah-Reum Oh, Do-Wan Kim, Young Un Kim, Young Du Choi, KyeongJin Kim
BMB Reports.2026; 59(9): 418. CrossRef

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Original Article

Hepatic neoplasm

KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression: Young Hoon Jung, Yun Ji Lee, Tam Dao, Kyung Hee Jung, Junjie Yu, Ah-Reum Oh, Yelin Jeong, HyunJoon Gi, Young Un Kim, Dongryeol Ryu, Michele Carrer, Utpal B. Pajvani, Sang Bae Lee, Soon-Sun Hong, KyeongJin Kim; Clin Mol Hepatol 2024;30(4):895-913.
Published online August 5, 2024; DOI: https://doi.org/10.3350/cmh.2024.0364

Background/Aims
Potassium channel tetramerization domain containing 17 (KCTD17) protein, an adaptor for the cullin3 (Cul3) ubiquitin ligase complex, has been implicated in various human diseases; however, its role in hepatocellular carcinoma (HCC) remains elusive. Here, we aimed to elucidate the clinical features of KCTD17, and investigate the mechanisms by which KCTD17 affects HCC progression.
Methods
We analyzed transcriptomic data from patients with HCC. Hepatocyte-specific KCTD17 deficient mice were treated with diethylnitrosamine (DEN) to assess its effect on HCC progression. Additionally, we tested KCTD17-directed antisense oligonucleotides for their therapeutic potential in vivo.
Results
Our investigation revealed the upregulation of KCTD17 expression in both tumors from patients with HCC and mouse models of HCC, in comparison to non-tumor controls. We identified the leucine zipper-like transcriptional regulator 1 (Lztr1) protein, a previously identified Ras destabilizer, as a substrate for KCTD17-Cul3 complex. KCTD17-mediated Lztr1 degradation led to Ras stabilization, resulting in increased proliferation, migration, and wound healing in liver cancer cells. Hepatocyte-specific KCTD17 deficient mice or liver cancer xenograft models were less susceptible to carcinogenesis or tumor growth. Similarly, treatment with KCTD17-directed antisense oligonucleotides (ASO) in a mouse model of HCC markedly lowered tumor volume as well as Ras protein levels, compared to those in control ASO-treated mice.
Conclusions
KCTD17 induces the stabilization of Ras and downstream signaling pathways and HCC progression and may represent a novel therapeutic target for HCC.

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Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models
Jack Leslie, Kishore A. Krishnamurthy, Indresh K. Gopalsamy, Patricia Inacio, Meritxell Huch, Suchira Gallage, Fiona Oakley, Michele Vacca
Nature Reviews Gastroenterology & Hepatology.2026; 23(4): 286. CrossRef
Functional food potential of Cornus officinalis for liver health: mechanistic evidence and perspectives
Bo Liu, Yi He, Xuan Ma, Chenrui Zhao, Qin Chen, Yundan Li, Jiangying Heng, Yu Zhang, Jing Jin, Feng Wang
Food Science and Human Wellness.2026; 15(2): 9250842. CrossRef
E3 Ubiquitin Ligases in MASH‐Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities
Ah‐Reum Oh, Yelin Jeong, Young Hoon Jung, Young Un Kim, HyunJoon Gi, Do‐Wan Kim, Young Du Choi, Sang Bae Lee, KyeongJin Kim
Liver International.2026;[Epub] CrossRef
Multifaceted roles of KCTD17 in cellular homeostasis and disease
Yelin Jeong, HyunJoon Gi, Young Hoon Jung, Ah-Reum Oh, Do-Wan Kim, Young Un Kim, Young Du Choi, KyeongJin Kim
BMB Reports.2026; 59(9): 418. CrossRef
Correspondence to editorial on “KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression”
Sang Bae Lee, KyeongJin Kim
Clinical and Molecular Hepatology.2025; 31(1): e78. CrossRef
Identification of KCTD17 as a Ras stabilizer in hepatocellular carcinoma: Editorial on “KCTD17-mediated Ras stabilization promotes hepatocellular carcinoma progression”
Rainbow Wing Hei Leung, Terence Kin Wah Lee
Clinical and Molecular Hepatology.2025; 31(1): 304. CrossRef
The ubiquitin code of RAS proteins: Decoding its role in cancer progression
Yedan Shi, Yong Shen, Xiuyuan Zhang, Ning Zhu, Yuwei Ding, Ying Yuan, Juan Wang
iScience.2025; 28(8): 113029. CrossRef
Structure, Function, and Role of KCTD9 in Human Diseases
宗军刘
Journal of Clinical Personalized Medicine.2025; 04(04): 33. CrossRef
Hepatocyte KCTD17-mediated SERPINA3 inhibition determines liver fibrosis in metabolic dysfunction-associated steatohepatitis
Yelin Jeong, Ah-Reum Oh, Young Hoon Jung, Kyung Hee Jung, Seongju Lee, Michele Carrer, Sang Bae Lee, Luca Valenti, Utpal B. Pajvani, KyeongJin Kim
Experimental & Molecular Medicine.2025; 57(8): 1673. CrossRef
Value of CD8+ T cell-related genes and IL-6/STAT3 signaling pathway in the prognosis of HCC and experimental investigation
Yuan Wu, Xiaoli Liu, Lihua Yu, Huiwen Yan, Yuqing Xie, Qing Pu, Yuling Liang, Yaxian Kong, Zhiyun Yang
International Journal of Biological Macromolecules.2025; 332: 148526. CrossRef
Wild-type KRAS activation drives evasion of interferon-mediated immunity and resistance to immunotherapy in hepatocellular carcinoma
Martina Mang Leng Lei, Carmen Oi Ning Leung, Rainbow Wing Hei Leung, Xue Qian Wu, Katherine Po Sin Chung, Catherine Yu Jia Gu, Mandy Sze Man Chan, Wing Ki Chau, Quan Hua Mu, Kai Yu Ng, Man Tong, Jing Ping Yun, Jia Ming Nickolas Teo, Guang Sheng Ling, Patr
Nature Communications.2025;[Epub] CrossRef

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Snapshot

Steatotic liver disease

Evaluating the therapeutic efficacy of NAD supplementation in management of metabolic dysfunction-associated steatotic liver disease: Key considerations: Xinyi Lu, Rui Yang, Yu Chen, Daozhen Chen; Clin Mol Hepatol 2024;30(3):582-584.
Published online December 29, 2023; DOI: https://doi.org/10.3350/cmh.2023.0555

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β-Nicotinamide Mononucleotide protects against endotoxemia-induced myocardial injury through Sirt5-dependent desuccinylation of succinate dehydrogenase
Hongmei Tao, Qian Dong, Yang Long, Ling Liu, Shu Qin, Yu Wang
European Journal of Pharmacology.2026; 1015: 178562. CrossRef
Immunonutrition: Another Player on the MASLD Field
Iván López-Méndez, Misael Uribe, Eva Juárez-Hernández
International Journal of Molecular Sciences.2025; 26(18): 8928. CrossRef

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Review

RNA interference as a novel treatment strategy for chronic hepatitis B infection: Rex Wan-Hin Hui, Lung-Yi Mak, Wai-Kay Seto, Man-Fung Yuen; Clin Mol Hepatol 2022;28(3):408-424.
Published online February 17, 2022; DOI: https://doi.org/10.3350/cmh.2022.0012

Abstract
PDF

Chronic hepatitis B (CHB) is a major cause of liver-related morbidity and mortality. Functional cure of CHB, defined as sustainable hepatitis B surface antigen (HBsAg) seroclearance, is associated with improved clinical outcomes. However, functional cure is rarely attainable by current treatment modalities. RNA interference (RNAi) by small-interfering RNA (siRNA) and anti-sense oligonucleotide (ASO) has been studied as a novel treatment strategy for CHB. RNAi targets post-transcriptional messenger RNAs and pregenomic RNAs to reduce hepatitis B virus (HBV) antigen production and viral replication. By reducing viral antigens, host immune reconstitution against HBV may also be attained. Phase I/II trials on siRNAs have demonstrated them to be safe and well-tolerated. siRNA is effective when given in monthly doses with different total number of doses according to different trial design, and can lead to sustainable dose-dependent mean HBsAg reduction by 2–2.5 log. Incidences of HBsAg seroclearance after siRNA therapy have also been reported. ASOs have also been studied in early phase trials, and a phase Ib study using frequent dosing regimen within 4 weeks could achieve similar HBsAg reduction of 2 log from baseline. Given the established efficacy and safety of nucleos(t) ide analogues (NAs), future RNAi regimens will likely include NA backbone. While the current evidence on RNAi appears promising, it remains undetermined whether the potent HBsAg reduction by RNAi can result in a high rate of HBsAg seroclearance with durability. Data on RNAi from phase IIb/III trials are keenly anticipated.

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Wenjing Zai, Min Yang, Kuan Jiang, Juan Guan, Huijing Wang, Kongying Hu, Chao Huang, Jieliang Chen, Wei Fu, Changyou Zhan, Zhenghong Yuan
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Mehrangiz Dezhbord, Seong Ho Kim, Soree Park, Da Rae Lee, Nayeon Kim, Juhee Won, Ah Ram Lee, Dong-Sik Kim, Kyun-Hwan Kim
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Editorial

Steatotic liver disease

An analysis of polygenic risk scores for non-alcoholic fatty liver disease: Dae Won Jun; Clin Mol Hepatol 2021;27(3):446-447.
Published online May 21, 2021; DOI: https://doi.org/10.3350/cmh.2021.0133

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Original Articles

Hepatic neoplasm

Meta-analysis of the correlation between the rs17401966 polymorphism in kinesin family member 1B and susceptibility to hepatitis B virus related hepatocellular carcinoma: Mingkuan Su, Jianfeng Guo, Jiancheng Huang; Clin Mol Hepatol 2017;23(2):138-146.
Published online April 21, 2017; DOI: https://doi.org/10.3350/cmh.2016.0083

Abstract
PDF

Background/Aims
The association between the kinesin family member 1B (KIF1B) gene polymorphism and the risk of hepatitis B virus-related hepatocellular carcinoma (HCC) has been investigated in many peer-reviewed studies. However, scholars have failed to replicate these results in validation tests. The purpose of the present study was to explore whether the KIF1B rs17401966 polymorphism was associated with susceptibility to HCC.
Methods
The results of case-controlled studies on the correlation between the KIF1B rs17401966 polymorphism and HCC susceptibility were collected using Google Scholar and the EMBASE, PubMed and CNKI databases. Based on inclusion and exclusion criteria, 5 papers with a total of 12 cohorts were included in this study.
Results
The 12 cohorts were integrated, and the results showed that the rs17401966 polymorphism reduced the risk for HCC under the allele, heterozygous, homozygous, and dominant models but not under the additive or recessive models. Moreover, the merged results showed strong heterogeneity, and the cumulative meta-analysis results were unreliable. A genetic differentiation analysis of the 12 cohorts found different degrees of genetic differentiation between the 5 cohorts in Zhang et al.’s study and the cohorts in the other studies. We further divided the 12 study cohorts into 2 subgroups based on fixation index value; however, the results of that analysis were inconsistent.
Conclusions
The results of this meta-analysis were not able to verify the association between the KIF1B rs1740199 polymorphism and HCC risk. Therefore, a well-designed, large-scale, multicenter validation study is needed to confirm the relationship.

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Eithar Mohamed, Sara Goodman, Leah Cooksey, Daniel M. Fletcher, Olivia Dean, Viktoriya B. Boncheva, Ken I. Mills, Kim H. Orchard, Barbara-ann Guinn
Onco.2025; 5(2): 19. CrossRef
The role of kinesin family members in hepatobiliary carcinomas: from bench to bedside
Kai Zhao, Xiangyu Li, Yunxiang Feng, Jianming Wang, Wei Yao
Biomarker Research.2024;[Epub] CrossRef
Association between KIF1B rs17401966 genetic polymorphism and hepatocellular carcinoma susceptibility: an updated meta-analysis
Ying-ying Luo, Hong-peng Zhang, Ai-long Huang, Jie-li Hu
BMC Medical Genetics.2019;[Epub] CrossRef
Host and Viral Genetic Variation in HBV-Related Hepatocellular Carcinoma
Ping An, Jinghang Xu, Yanyan Yu, Cheryl A. Winkler
Frontiers in Genetics.2018;[Epub] CrossRef

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Viral hepatitis

No association between the IL28B SNP and response to peginterferon plus ribavirin combination treatment in Korean chronic hepatitis C patients: Nae-Yun Heo, Young-Suk Lim, Woochang Lee, Minkyung Oh, Jiyun An, Danbi Lee, Ju Hyun Shim, Kang Mo Kim, Han Chu Lee, Yung Sang Lee, Dong Jin Suh; Clin Mol Hepatol 2014;20(2):177-184.
Published online June 30, 2014; DOI: https://doi.org/10.3350/cmh.2014.20.2.177

Abstract
PDF

Background/Aims

There are few available data regarding the association between the single nucleotide polymorphisms (SNPs) of the gene encoding interleukin 28B (IL28B) and a sustained virologic response (SVR) to peginterferon (PEG-IFN) plus ribavirin (RBV) therapy in Korean chronic hepatitis C patients.

Methods

This was a retrospective cohort study of 156 patients with chronic hepatitis C virus (HCV) infection who received combination treatment of PEG-IFN plus RBV. Blood samples from these patients were analyzed to identify the IL28B SNPs at rs12979860, rs12980275, rs8099917, and rs8103142. Association analyses were performed to evaluate the relationships between each IL28B SNP and SVRs.

Results

Seventy six patients with HCV genotype 1 and 80 with genotype non-1 were enrolled. The frequencies of rs12979860 CC and CT genotypes were 90.4% and 9.6%, respectively; those of rs12980275 AA and AG genotypes were 87.2% and 12.8%, respectively; those of rs8099917 TT and TG genotypes were 92.3% and 7.7%, respectively; and those of rs8103142 TT and CT genotypes were 90.4% and 9.6%, respectively. Among the patients with HCV genotype 1, the SVR rates were 69.7% and 80.0% for rs12979860 CC and CT, respectively (P=0.71). Among the HCV genotype non-1 patients, SVR rates were 88.0% and 100% for rs12979860 CC and CT (P=1.00), respectively.

Conclusions

Genotypes of the IL28B SNP that are known to be favorable were present in most of the Korean patients with chronic hepatitis C in this study. Moreover, the IL28B SNP did not influence the SVR rate in either the HCV genotype 1 or non-1 patients. Therefore, IL28B SNP analysis might be not useful for the initial assessment, prediction of treatment outcomes, or treatment decision-making of Korean chronic hepatitis C patients.

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IL28B gene polymorphism rs12979860, but not rs8099917, contributes to the occurrence of chronic HCV infection in Uruguayan patients
Natalia Echeverría, Daniela Chiodi, Pablo López, Adriana Sanchez Ciceron, Jenniffer Angulo, Marcelo López-Lastra, Paola Silvera, Adrian Canavesi, Carla Bianchi, Valentina Colistro, Juan Cristina, Nelia Hernandez, Pilar Moreno
Virology Journal.2018;[Epub] CrossRef
The impact of genetic variation in IL28B, IFNL4 and HLA genes on treatment responses against chronic hepatitis C virus infection
Fatemeh Sakhaee, Morteza Ghazanfari, Farzam Vaziri, Fatemeh Rahimi Jamnani, Mehdi Davari, Safoora Gharibzadeh, Roohollah Fateh, Farid Abdolrahimi, Shahin Pourazar Dizaji, Abolfazl Fateh, Seyed Davar Siadat
Infection, Genetics and Evolution.2017; 54: 330. CrossRef
Immunological dynamics associated with rapid virological response during the early phase of type I interferon therapy in patients with chronic hepatitis C
Jae-Won Lee, Won Kim, Eun-Kyung Kwon, Yuri Kim, Hyun Mu Shin, Dong-Hyun Kim, Chan-Ki Min, Ji-Yeob Choi, Won-Woo Lee, Myung-Sik Choi, Byeong Gwan Kim, Nam-Hyuk Cho, Eui-Cheol Shin
PLOS ONE.2017; 12(6): e0179094. CrossRef
IL28B rs12980275 variant as a predictor of sustained virologic response to pegylated-interferon and ribavirin in chronic hepatitis C patients: A systematic review and meta-analysis
Hao Zheng, Man Li, Bing Chi, Xiao-xue Wu, Jia Wang, Dian-Wu Liu
Clinics and Research in Hepatology and Gastroenterology.2015; 39(5): 576. CrossRef

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Review

Viral hepatitis

Options for the management of antiviral resistance during hepatitis B therapy: reflections on battles over a decade: Hyung Joon Yim, Seong Gyu Hwang; Clin Mol Hepatol 2013;19(3):195-209.
Published online September 30, 2013; DOI: https://doi.org/10.3350/cmh.2013.19.3.195

Abstract
PDF

Although much advancement has been achieved in the treatment of chronic hepatitis B, antiviral resistance is still a challenging issue. Previous generation antiviral agents have already developed resistance in a number of patients, and it is still being used especially in resource limited countries. Once antiviral resistance occurs, it predisposes to subsequent resistance, resulting in multidrug resistance. Therefore, prevention of initial antiviral resistance is the most important strategy, and appropriate choice and modification of therapy would be the cornerstone in avoiding treatment failures. Until now, management of antiviral resistance has been evolving from sequential therapy to combination therapy. In the era of tenofovir, the paradigm shifts again, and we have to decide when to switch and when to combine on the basis of newly emerging clinical data. We expect future eradication of chronic hepatitis B virus infection by proper prevention and optimal management of antiviral resistance.

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Original Article

Transcriptional profiling and Wnt signaling activation in proliferation of human hepatic stellate cells induced by PDGF-BB: HyeWon Shin, M.S., Soo Young Park, M.S., Kyoung Bun Lee, M.D., Eun Shin, M.D., Suk Woo Nam, Ph.D.1, Jung Young Lee, M.D.1, Ja-June Jang, M.D.; Korean J Hepatol 2009;15(4):486-495.
Published online December 31, 2009; DOI: https://doi.org/10.3350/kjhep.2009.15.4.486

Abstract
PDF

Background/Aims
This study aimed to better understand gene expression profiles of human hepatic stellate cell (HSC) activation and the relationship with the Wnt signaling pathway. Methods: The global transcript levels in platelet derived growth factor-BB (PDGF-BB)-stimulated hTERT HSCs were analyzed using oligonucleotide microarrays. Oligonucleotide microarrays with 19K human oligo chips were performed to obtain gene expression profiles associated with proliferation in human hTERT HSCs. The microarray data was verified by real time quantitative PCR and expression of the components of Wnt signaling was analyzed by Western blot. Results: Microarray data showed 243 up-regulated and 265 down-regulated genes in PDGF-BB-treated HSCs. The changes in expression of glypican3 and BH3 interacting domain death agonist (BID) mRNA in real time quantitative PCR, especially among the highly up- or down-regulated genes, were statistically consistent with the microarray data. The Wnt signaling pathway components, frizzled10 (FZD10) and calcium/calmodulin-dependent protein kinase II alpha (CAMK2A), showed increased expression in the short time course microarray and the up-regulation of FZD10 also occurred at the protein level. Our data showed various gene expression profiles during activation of human HSC. Conclusions: The up-regulated expression of FZD10 and CAMK2A suggests that the Wnt/Ca²⁺ signaling pathway is active in hTERT HSCs and may participate in HSC activation and proliferation. (Korean J Hepatol 2009;15:486-495)

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Review

Genetic epidemiological study on single nucleotide polymorphisms associated with hepatocellular carcinoma in patients with chronic HBV infection: Yoon Jun Kim , Hyo Suk Lee; Korean J Hepatol 2009;15(1):7-14.
Published online March 31, 2009; DOI: https://doi.org/10.3350/kjhep.2009.15.1.7

Abstract
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Hepatocellular carcinoma (HCC) is associated with hepatitis B virus (HBV) as an etiologic agent in 80% of cases, and is the major cause of death among HBV carriers. Family history of HCC is a known risk factor for the development of HCC among chronically HBV infected patients, therefore, genetic factors are likely to modify the risk of HCC. However, the genetic factors that determine progression to HCC remain mostly to be recovered. It is estimated that there are millions of single nucleotide polymorphisms (SNPs) within human genome and they are likely to explain much of the genetic diversity of individuals. In this review, the natural history of HBV infection and host genetic factors related to HCC, study design and target gene selection for the detection of SNPs related to the occurrence of HCC were discussed. Also, several SNPs or haplotypes, which were reportedly associated with increased or reduced risk of HCC occurrence in patients with chronic HBV infection, were reviewed. Especially, recent studies in Korea, one of the HBV endemic areas, were discussed. Screening of these polymorphisms might be useful in clinical practice to stratify the lower or higher risk group for HCC and might modify the design of HCC surveillance programs in patients with chronic HBV infection, if further genetic susceptibilities are identified. The ongoing studies of the distributions and functions of the implicated allele polymorphisms will not only provide insight into the pathogenesis of HCC, but may also provide a novel rationale for new methods of diagnosis and therapeutic strategies. (Korean J Hepatol 2008;15:7-14)

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Original Article

Persistent Negative Anti-HBc in Chronic Hepatitis B Virus Carrier -Clinical Review, HBcAg and Nucleotide Sequence of It`s Epitope in HLA A2 Heterozygotes-: Jae Heung Kim,Haak Cheoul Kim; Korean J Hepatol 1999;5(2):105-115.

Abstract
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Background/Aims
: HBcAg is the most immunogenic HBV component and anti-HBc usually persists irrespective of ongoing liver disease or clearance of the virus in human. Therefore anti-HBc is considered as the most sensitive and occasionally the only marker of the HBV infection. Nevertheless, there are a few HBsAg carrier with persistent negative anti-HBc. The epitope which responds to HBcAg is recently defined in HLA A2 from acute viral hepatitis patient due to HBV. So we studied the clinical and laboratory features and nucleotide sequence of HBcAg corresponding to HLA A2 in the HBsAg carrier with persistent negative anti-HBc. Methods : The subject of these study consists of eight HBsAg chronic carriers with persistent negative anti-HBc. We followed up the clinical features and serological markers of HBV infection and determined the amount of humoral immunoglobulin, HBV DNA and HBcAg when we performed the HLA class I typing and sequencing analysis of core of HBV. Control cases were selected from 3 HLA A2 heterozygote cases with chronic HBsAg carriers with anti-HBc. Results : All subjects had the HBsAg persistently and good health conditions with normal ranges of aminotransferase and humoral immunoglobulin. One of them was converted to anti-HBc-positive during follow-up period. The level of HBV DNA in serum was higher than 1.2 pg/mL in 7 of 8 chronic HBV carriers. There was a trend of differences between chronic anti-HBc negative carriers and converted one case to anti-HBc positive in the serum of HBcAg and HBV DNA(p=0.06). But strong positive correlation was observed between the amount of HBcAg and HBV DNA in sera. The core portion of HBV was amplified in 4 of 6 HLA A2 heterozygotes by single PCR. When sequenced the PCR products of the above 4 chronic anti-HBc negative HBV carriers and 3 control cases directly, there were no significant difference in the nucleotide and amino acid sequence at the HBcAg epitope which corresopond to class 1 HLA A2. Conclusions : Our results show that persistent anti-HBc negative chronic HBV carriers may be caused by large amounts of HBV DNA and HBcAg in their sera and not by variants of HBV. These suggested that active viral replication was going on, but are undetectable by the available commercial tests due to binding with excessive amount of HBcAg in the HBV carriers with persistent negative anti-HBc. (Korean J Hepatol 1999;5:105－115)