HSIANG-PO HUANGHONG-YUAN HSUCHI-LING CHENYEN-HSUAN NIHURNG-YI WANGTsuei D.-J.Chiang C.-L.Tsai Y.-C.HUEY-LING CHENMEI-HWEI CHANG2022-01-252022-01-2520100031-3998https://www.scopus.com/inward/record.uri?eid=2-s2.0-73449131849&doi=10.1203%2fPDR.0b013e3181c1b0b7&partnerID=40&md5=eafabc5062f28602358d9659165df223https://scholars.lib.ntu.edu.tw/handle/123456789/593454The 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. Copyright ? 2009 International Pediatric Research Foundation, Inc.[SDGs]SDG3adolescent; article; child; clinical article; controlled study; female; gene deletion; gene sequence; genotype; hepatitis B; Hepatitis B virus; human; liver cell carcinoma; male; multivariate logistic regression analysis; nonhuman; polymerase chain reaction; priority journal; risk factor; school child; Adolescent; Base Sequence; Carcinoma, Hepatocellular; Child; DNA Primers; Female; Hepatitis B Surface Antigens; Hepatitis B virus; Humans; Liver Neoplasms; Male; Polymerase Chain Reaction; Protein Precursors; Risk Factorsjournal article10.1203/PDR.0b013e3181c1b0b7198162382-s2.0-73449131849