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Abe K et al. – The HBV pre–S2 deletion mutant at nt 4–57 which has a CD8 T–cell epitope could be responsible for the emergence and aggressive outcome of childhood HCC. Determination of this hotspot mutation in the pre–S2 region could be a useful index for predicting the clinical outcome of HCC development.

Exclusive Author Commentary
Kenji Abe, 09/24/09

The pathogenesis of chronic hepatitis B/C and its malignant transformation in children on the other hand, is poorly understood. Childhood HCC, however, is a real concern as most of them behave aggressively and have a high mortality rate. Understanding hepatocarcinogenesis in children is important, because childhood HCCs can provide evidence of a direct role of HBV in carcinogenesis, when many risk factors such as alcohol, smoking, diabetes and obesity can still be excluded. To address these issues, we conducted a retrospective study of childhood HCCs in Asia which is highly endemic for HBV/HCV. In this study, we could identify a hot spot mutation in the pre-S2 gene of HBV which could have an important role in hepatocarcinogenesis in children.

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