Temporal relationship between hepatitis B virus enhancer II/basal core promoter sequence variation and risk of hepatocellular carcinoma

Chou, Yi-Chun; Yu, Ming‐Whei; Wu, Chin-Chin; Yang, Shi-Yi; Lin, Chih–Lin; Liu, Chun‐Jen; Shih, Wei-Liang; Chen, Pei‐Jer; Liaw, Yun–Fan; Chen, Chien-Jen

doi:10.1136/gut.2006.114066

Cited by 101 publications

(101 citation statements)

References 35 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%

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%

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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“…26 By characterizing the HBV genome sequences derived from patients' serum, several studies have illustrated that various virological factors are closely associated with hepatocarcinogenesis, including serum HBV-DNA concentration, genotype, and the presence of a basal core promoter mutation. 27 Furthermore, by performing cell-based and animalbased experiments, several viral proteins have been shown to be implicated in the oncogenesis of liver cancer, including X proteins, large surface proteins, and pre-S deletion mutants. 23,28,29 Despite convincing evidence provided by these studies, the link between HBV and carcinogenesis has not been carefully investigated by examining the prognostic value of these virological factors in a postoperative model.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus-DNA level and basal core promoter A1762T/G1764A mutation in liver tissue independently predict postoperative survival in hepatocellular carcinoma

Yeh

et al. 2010

Hepatology

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Hepatitis B virus (HBV) is a major etiological factor of hepatocellular carcinoma (HCC). However, the postoperative prognostic value of the virological factors assayed directly from liver tissue has never been investigated. To address this issue, 185 liver samples obtained from the noncancerous part of surgically removed HBV-associated HCC tissues were subjected to virological analysis. Assayed factors included the amount of HBV-DNA in the liver tissues; genotype; and the presence of the HBV precore stop codon G1896A mutation, basal core promoter A1762T/G1764A mutation, and pre-S deletions/stop codon mutation. All virological factors and clinicopathological factors were subjected to Cox proportional hazard model analysis to estimate postoperative survival. It was found that an HBV-DNA level >3.0 3 10 7 copies/g of liver tissue and the presence of the basal core promoter mutation independently predicted disease-free (adjusted hazard ratio 1. Kaplan-Meier survival analysis indicated that in-frame, short stretch (<100 bp) pre-S deletions, but not large fragment (>100 bp) pre-S deletions, were significantly associated with poorer disease-free (P 5 0.005) and overall (P 5 0.020) survival. A hot deletion region located between codons 107 and 141 of the pre-S sequence was identified for the short stretch pre-S deletion mutants. Conclusion: The amount of HBV-DNA in liver tissue and the presence of the basal core promoter mutation were two independent predictors for postoperative survival in HCC. A short stretch pre-S deletion located between codons 107 and 141 was strongly associated with a poorer postoperative prognosis. (HEPATOLOGY 2010;52:1922-1933 W orldwide, hepatocellular carcinoma (HCC) is the fifth most commonly diagnosed solid cancer and the third most common cause of cancer-related death.1 HCC is multifactorial in origin. The three most important causes are chronic hepatitis B virus (HBV) infection, chronic hepatitis C virus infection, and alcoholic liver disease.2,3 Other risk factors include old age, male sex, underlying chronic liver diseases, and most importantly, liver cirrhosis. [4][5][6] Aflatoxin exposure and diabetes have also been linked to the development of HCC. 7In areas such as Southeast Asia, where chronic hepatitis B continues to be highly prevalent, a correspondingly high incidence of HCC is found. 4 Furthermore, despite a successful vaccination program in Taiwan, HBV remains the major etiological factor of HCC in patients over 25 years of age. Consequently, much

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“…Thus, the baseline HBV mutations in combination are able to predict the occurrence of HCC in CHB patients [33] . Several longitudinal studies carried in China have also demonstrated that baseline A1762T/G1764A mutation increases the risk of HCC in chronic HBV carriers or CHB patients [34][35][36][37] . Among the HCC-risk HBV mutations, the A1762T/G1764A is usually detected in the early stage in young adolescents, while other mutations including T1753V, C1653T, G1899A, and preS deletion appear only at the late stage of chronic HBV infection [12,38] .…”

Section: "Dead-end" Evolution Of Hbvmentioning

confidence: 98%

Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

Cao¹

2017

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How to cite this article: Cao GW. Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis. Hepatoma Res 2017;3:241-59.Non-resolving inflammation, which may be maintained by infection, pollution, and metabolic stimulants and their interactions with immunogenetic predisposition, provides a fertile field for cancer development. This is strongly evident in hepatocellular carcinoma. Here, the framework of a hypothesis called Cancer Evo-Dev is presented, based on the advances in hepatitis B virusinduced hepatocarcinogenesis. Several aspects central to this theory are as follows: (1) immune imbalance caused by the interaction of immunogenetic predispositions and hepatitis B virus infection maintains non-resolving inflammation; (2) active inflammation executants promote mutations in viral and host genomes via disbalancing mutagenic forces including cytidine deaminases and mutation-repairing forces including uracil-DNA glycosylases, thus promoting cancer-related somatic mutations and viral mutations; (3) a small percentage of the cells whose somatic mutations alter the survival signalling adapt to the inflammatory microenvironment, de-differentiate via demethylating role of cytidine deaminases, and reversely develop into tumor-initiating cells (TICs); (4) under the cultivation of some factors like POSTN from tumorinfiltrating fibroblasts and M2 macrophages, TICs acquire the stemness, cancer-stem cells obtain distinct metastatic and drug-resistant potentials under the selection pressure from distinct microenvironments; (5) glycolysis persistence in the presence of oxygen provides essential energy for cell survival and the raw material for DNA synthesis. Thus, cancer development is characterized by an evolutionary process of "mutation-selection-adaptation". The framework of Cancer Evo-Dev can be verified in other cancers. Cancer Evo-Dev lays theoretical foundation for understanding the mechanisms by which inflammation promotes cancer development, and it also plays a role in specific prophylaxis, prediction, and targeted treatment of cancers. Key words:Inflammation, hepatitis B virus, mutations, hepatoma, Cancer Evo-Dev ABSTRACTArticle history:

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Temporal relationship between hepatitis B virus enhancer II/basal core promoter sequence variation and risk of hepatocellular carcinoma

Abstract: HCC risk is associated with sequence variation in the EnhII/BCP regions of HBV, and persistence of at-risk sequence variants is critical for HCC development.

Cited by 101 publications

References 35 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-DNA level and basal core promoter A1762T/G1764A mutation in liver tissue independently predict postoperative survival in hepatocellular carcinoma

Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

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