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Carcinogenesis Advance Access originally published online on April 16, 2004
Carcinogenesis 2004 25(9):1593-1598; doi:10.1093/carcin/bgh172
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Carcinogenesis vol.25 no.9 © Oxford University Press 2004; all rights reserved.

ARTICLE

Role of hepatitis B virus genotypes Ba and C, core promoter and precore mutations on hepatocellular carcinoma: a case control study

Man-Fung Yuen1, Yasuhito Tanaka2, Masashi Mizokami2, John Chi-Hang Yuen1, Danny Ka-Ho Wong1, He-Jun Yuan1, Siu-Man Sum1, Annie On-On Chan1, Benjamin Chun-Yu Wong1 and Ching-Lung Lai1,3

1 Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong and 2 Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Kawasumi, Mizuho, Nagoya 467-8601, Japan

3 To whom correspondence should be addressed Email: hrmelcl{at}hkucc.hku.hk

The role of hepatitis B virus (HBV) genotypes, core promoter (CP) and precore mutants on hepatocellular carcinoma (HCC) is still controversial. We aimed to determine their role on the development and clinical features of HCC. HBV genotypes and CP/precore mutations were determined in 90 HCC patients and 180 matched control patients. In the 90 HCC patients, 22 (24.4%) and 68 (75.6%) had subtype Ba and genotype C, respectively. The prevalence of genotype C and CP mutations was significantly higher in HCC patients compared with controls (75.6 versus 57.8%, P = 0.004; 90.9 versus 74.8%, respectively, P = 0.007). Among carriers of genotype C, 91.8% of the HCC patients and 88.8% of controls had CP mutations. Among carriers of subtype Ba, HCC patients had a higher prevalence of CP mutations compared with controls (88.2 versus 54.5%, respectively, P = 0.02). By logistic regression analysis, the only factor associated with HCC was a mutation of the CP region (P = 0.032). There were no differences in the clinical features on presentation, the chance of receiving treatment and the cumulative survival rate for chemoembolization-treated patients between patients with subtype Ba and genotype C. There was too small a number of CP wild-type to do a similar comparison with CP mutants. In conclusion, there was a significantly higher prevalence of both genotype C and CP mutations in patients with HCC. The association between HBV genotype C and HCC was probably not genuine but was due to the high percentage of CP mutations in patients with genotype C.


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