| Literature DB >> 19816238 |
Hsiang-Po Huang1, Hong-Yuan Hsu, Chi-Ling Chen, Yen-Hsuan Ni, Hurng-Yi Wang, Daw-Jen Tsuei, Cheng-Lun Chiang, Yi-Chen Tsai, Huey-Ling Chen, Mei-Hwei Chang.
Abstract
UNLABELLED: The cause of early oncogenesis in hepatitis B virus (HBV)-related childhood hepatocellular carcinoma (HCC) remains unclear. This study investigated whether pre-S deletion of HBV is related to childhood HCC. By using nested polymerase chain reaction, we compared the pre-S sequence of HBV from sera of children with HCC against control children with similar chronic HBV infection. The HBV in sera of children with HCC had a significantly higher rate of pre-S deletion than that of children with chronic HBV infection (p = 0.008). All except one of the pre-S deletions from the HCC group involved the pre-S2 region, whereas no pre-S2 deletion was found in the chronic HBV group (p = 0.003). There was a trend whereby genotype-C sera had a higher rate of pre-S2 deletion than genotype-B sera (p = 0.11). A multivariate logistic regression model revealed that pre-S deletion was an independent risk factor for HCC in children (odds ratio: 36.69, p = 0.015). In conclusion, pre-S2 deletion does not need to take decades to occur; its presence in nearly half of children with HCC, in contrast to its absence in children with chronic HBV infection, suggests a link between pre-S2 deletion and HCC development in children. ABBREVIATIONS: :Entities:
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Year: 2010 PMID: 19816238 DOI: 10.1203/PDR.0b013e3181c1b0b7
Source DB: PubMed Journal: Pediatr Res ISSN: 0031-3998 Impact factor: 3.756