Detection of hepatic oxidative DNA damage in patients with hepatoblastoma and children with non-neoplastic disease

✍ Scribed by Ikeda, Hitoshi ;Hirato, Junko ;Suzuki, Norio ;Kuroiwa, Minoru ;Maruyama, Kenichi ;Tsuchida, Yoshiaki

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 265 KB
• Volume: 37
• Category: Article
• ISSN: 0098-1532
• DOI: 10.1002/mpo.1243

✦ Synopsis

Abstract

Background

The authors have revealed a significant association between hepatoblastoma and low birth weight. This study was done to explore the evidence that liver cells were oxidatively damaged, based on the hypothesis that oxidative damage to DNA is involved in the development of hepatoblastoma in children of low birth weight.

Procedure

Oxidative DNA damage in the liver was examined by immunohistochemically detecting the presence of a DNA repair product, 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG), in five patients with hepatoblastoma and 14 children with non‐neoplastic disease.

Results

Positive staining for 8‐OHdG was observed in all five patients with hepatoblastoma. Distribution of 8‐OHdG positivity was diffuse in the intralobular area in one patient and was restricted to the periportal area of the lobules in four patients. There was no apparent correlation between birth weight of the patients, histological findings in the liver, and the distribution of 8‐OHdG positivity. In children with non‐neoplastic disease, 8‐OHdG was detected in nine of 14 patients, and 8‐OHdG was positive in the intralobular area of the liver parenchyma except in one patient.

Conclusions

These results suggest that the cause of oxidative DNA damage in patients with hepatoblastoma may be different from the cause, extensive parenchymal damage to the liver, in children with non‐neoplastic disease, but the 8‐OHdG formation is not specific to hepatoblastoma patients of low birth weight. Further studies to elucidate the true reason for the high incidence of hepatoblastoma in children of low birth weight are necessary. Med Pediatr Oncol 2001; 37:505–510. © 2001 Wiley‐Liss, Inc.