Hepatocellular carcinoma and hepatitis B virus

被引：226

作者：

Chan, HLY ^{[1
]}

Sung, JJY ^{[1
]}

机构：

[1] Prince Wales Hosp, Dept Med & Therapeut, Shatin, Hong Kong, Peoples R China

来源：

SEMINARS IN LIVER DISEASE | 2006年 / 26卷 / 02期

基金：

美国国家卫生研究院;

关键词：

hepatitis B virus; hepatocellular carcinoma; gene; mutation; DNA;

D O I：

10.1055/s-2006-939753

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Chronic hepatitis B is the most common cause of hepatocellular carcinoma (HCC) in Asia. Integration of hepatitis B virus (HBV) genome is likely an early event of carcinogenesis. The integrated HBV genome may activate neighboring cellular genes directly to offer a selective growth advantage to the liver cells. Production of hepatitis B X protein can act as a transactivator on various cellular genes for tumor development. Hepatic inflammation and cirrhosis also favors the process of carcinogenesis. Various viral factors associated with hepatocellular carcinoma development include HBV genotype, basal core promoter mutations, and high viral load. Polymorphisms at the androgen receptor-regulating genes and cytokine genes are possible host factors associated With HCC. This review article summarizes the pathogenesis of HBV-related carcinogenesis and the viral and host factors that may increase the risk of HCC development.

引用

页码：153 / 161

页数：9

共 125 条

[31]

FUJIMOTO Y, 1994, CANCER RES, V54, P281

[32] Genetic control of the circulating concentration of transforming growth factor type β1 [J].

Grainger, DJ ;

Heathcote, K ;

Chiano, M ;

Snieder, H ;

Kemp, PR ;

Metcalfe, JC ;

Carter, ND ;

Spector, TD .

HUMAN MOLECULAR GENETICS, 1999, 8 (01) :93-97

[33] Downregulation of DNA excision repair by the hepatitis B virus-x protein occurs in p53-proficient and p53-deficient cells [J].

Groisman, IJ ;

Koshy, R ;

Henkler, F ;

Groopman, JD ;

Alaoui-Jamali, MA .

CARCINOGENESIS, 1999, 20 (03) :479-483

[34] Epidemiology of hepatitis B infection in the Western Pacific and South East Asia [J].

Gust, ID .

GUT, 1996, 38 :S18-S22

[35]

Heneghan Michael A, 2003, Int J Gastrointest Cancer, V34, P19

[36] Transcriptional regulation of the telomerase hTERT gene as a target for cellular and viral oncogenic mechanisms [J].

Horikawa, I ;

Barrett, JC .

CARCINOGENESIS, 2003, 24 (07) :1167-1176

[37] Long-term outcome after spontaneous HBeAg seroconversion in patients with chronic hepatitis B [J].

Hsu, YS ;

Chien, RN ;

Yeh, CT ;

Sheen, IS ;

Chiou, HY ;

Chu, CM ;

Liaw, YF .

HEPATOLOGY, 2002, 35 (06) :1522-1527

[38] Identification of chronic hepatitis B patients without significant liver fibrosis by a simple noninvasive predictive model [J].

Hui, AY ;

Chan, HLY ;

Wong, VWS ;

Liew, CT ;

Chim, AML ;

Chan, FKL ;

Sung, JJY .

AMERICAN JOURNAL OF GASTROENTEROLOGY, 2005, 100 (03) :616-623

[39] Sero-clearance of hepatitis B surface antigen in chronic carriers does not necessarily imply a good prognosis [J].

Huo, TI ;

Wu, JC ;

Lee, PC ;

Chau, GY ;

Lui, WY ;

Tsay, SH ;

Ting, LT ;

Chang, FY ;

Lee, SD .

HEPATOLOGY, 1998, 28 (01) :231-236

[40] Evaluation of hepatitis B and C viral markers: Clinical significance in Asian and Caucasian patients with hepatocellular carcinoma in the United States of America [J].

Hwang, SJ ;

Tong, MJ ;

Lai, PP ;

Ko, ES ;

Co, RL ;

Chien, D ;

Kuo, G .

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 1996, 11 (10) :949-954

← 1 2 3 4 5 6 7 8 9 10 →