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Download PDF by George F. Vande Woude (ed.), George Klein (ed.): Advances in Cancer Research, Vol. 108

By George F. Vande Woude (ed.), George Klein (ed.)

ISBN-10: 012380888X

ISBN-13: 9780123808882

Offers worthwhile info at the intriguing and fast-moving box of melanoma research. Outstanding and unique studies are offered on a number of themes.

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Extra info for Advances in Cancer Research, Vol. 108

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These factors are found to act synergistically to induce disease progression and increased risk of cirrhosis and HCC (Table I). Table I Factors Associated with the Development of Hepatocellular Carcinoma in Patients with Chronic Hepatitis B Virus Infection Virus Persistently high HBV replication Genotype (C > B, D > A) Specific HBV mutants (core promoter mutant, pre-S deletion) Host Male gender Advanced age or longer duration of infection Presence of cirrhosis Family history of HCC Ethnicity (Asian, African > Caucasian) Genetic alteration Diabetes mellitus Obesity Hepatic steatosis Repeated hepatitis flare Environmental Concurrent HCV, HDV, or HIV infection Alcohol drinking Cigarette smoking Aflatoxin exposure Betel nut chewing HCC, hepatocellular carcinoma; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis D virus; HIV, human immunodeficiency virus.

02). In addition, the prevalence of BCP A1762T/ G1764A mutant was higher in HCC patients with genotypes B and C. , 2006). Taking these lines of evidence together, BCP A1762T/G1764A mutation seems to play an important role in the pathogenesis of liver disease progression and serves as the strongest viral factor associated with HCC risk in HBV carriers. The biological mechanisms involved in BCP A1762T/G1764A mutationrelated hepatocarcinogenesis remain to be established. , 2008). In contrast, the promoter activity of HBV strains isolated from HCC patients was increased when 1762T and 1764A are reversely mutated into 1762A and 1764G, respectively.

Taken together, a dual change of A1762T/ G1764A in BCP will not only diminish the production of HBeAg, enhance viral replication and lead to increased host immune response but also induce an amino acid change in the X protein to promote hepatocarcinogenesis. Clinically, the role of precore G1896A stop codon mutation in disease progression remains debatable. , 2008) showed precore G1896A stop codon mutation may reduce the risk of HCC in HBV carriers (Table III). 37 Recent Advances in the Research of Hepatitis B 1613 1849 Core promoter Upstream regulatory region Basal core promoter 1742 Enhancer II 1627 1774 Box a 1644 Box b 1666 1701 1713 1653 GTCTTACATAAGACGACTCT 1752/1753 1762/1764/1766 GATTAGGTTAAAGGTCTTT C V I T HB-X protein L H K H94Y R T L K A G V I127N/S/T K130M V131I Fig.

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Advances in Cancer Research, Vol. 108 by George F. Vande Woude (ed.), George Klein (ed.)

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