Hepatitis B virus induced hepatocellular carcinoma

被引：147

作者：

Chemin, I. ^{[1
]}

Zoulim, F.

机构：

[1] INSERM, U871, F-69003 Lyon, France

来源：

CANCER LETTERS | 2009年 / 286卷 / 01期

关键词：

Hepatitis B; Occult infections; Natural history; Hepatocellularcinoma; UNFOLDED PROTEIN RESPONSE; OCCULT HBV INFECTION; SURFACE-ANTIGEN; MOLECULAR EPIDEMIOLOGY; ANTIVIRAL THERAPY; OXIDATIVE STRESS; UNKNOWN ETIOLOGY; TRANSGENIC MICE; LIVER-DISEASE; RISK-FACTOR;

D O I：

10.1016/j.canlet.2008.12.003

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

A number of risk factors appear to play a role in Hepatocellularcinoma (HCC), HBV infection being one of the most important. Chronic inflammation and cytokines are key determinants in the development of fibrosis and liver cell proliferation. HBV DNA integration and/or expression of HBV proteins may have a direct effect on cellular functions. Occult hepatitis B virus infection is characterized by persistence of HBV DNA in hepatitis B surface antigen-negative individuals. There are evidences that occult HBV is a risk factor for the development of HCC and that the potential mechanisms whereby overt HBV might induce tumour formation are mostly maintained. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

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页码：52 / 59

页数：8

相关论文

共 59 条

[11] THE INFLUENCE OF AGE ON THE DEVELOPMENT OF THE HEPATITIS-B CARRIER STATE [J].

EDMUNDS, WJ ;

MEDLEY, GF ;

NOKES, DJ ;

HALL, AJ ;

WHITTLE, HC .

PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 1993, 253 (1337) :197-201

[12] Hepatocellular carcinoma in cirrhosis: Incidence and risk factors [J].

Fattovich, G ;

Stroffolini, T ;

Zagni, I ;

Donato, F .

GASTROENTEROLOGY, 2004, 127 (05) :S35-S50

[13]

FILIPPI P, 1988, VIRAL HEPATITIS LIVE, P632

[14] Mechanisms of disease: Hepatitis B virus infection - Natural history and clinical consequences [J].

Ganem, D ;

Prince, AM .

NEW ENGLAND JOURNAL OF MEDICINE, 2004, 350 (11) :1118-1129

[15] Molecular epidemiology of hepatitis B virus variants in nonhuman primates [J].

Grethe, S ;

Heckel, JO ;

Rietschel, W ;

Hufert, FT .

JOURNAL OF VIROLOGY, 2000, 74 (11) :5377-5381

[16] The role of hepatitis B virus integrations in the pathogenesis of human hepatocellular carcinoma [J].

Guerrero, RB ;

Roberts, LR .

JOURNAL OF HEPATOLOGY, 2005, 42 (05) :760-777

[17] EXTENSIVE OXIDATIVE DNA-DAMAGE IN HEPATOCYTES OF TRANSGENIC MICE WITH CHRONIC ACTIVE HEPATITIS DESTINED TO DEVELOP HEPATOCELLULAR-CARCINOMA [J].

HAGEN, TM ;

HUANG, S ;

CURNUTTE, J ;

FOWLER, P ;

MARTINEZ, V ;

WEHR, CM ;

AMES, BN ;

CHISARI, FV .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (26) :12808-12812

[18] Degradation of misfolded proteins prevents ER-derived oxidative stress and cell death [J].

Haynes, CM ;

Titus, EA ;

Cooper, AA .

MOLECULAR CELL, 2004, 15 (05) :767-776

[19] Viruses, endoplasmic reticulum stress, and interferon responses [J].

He, B .

CELL DEATH AND DIFFERENTIATION, 2006, 13 (03) :393-403

[20] The PreS2 activator MJBst of hepatitis B virus activates c-raf-1/Erk2 signaling in transgenic mice [J].

Hildt, E ;

Munz, B ;

Saher, G ;

Reifenberg, K ;

Hofschneider, PH .

EMBO JOURNAL, 2002, 21 (04) :525-535

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