Overexpression of the oncoprotein p53 in primary hepatic tumors of childhood does not correlate with gene mutations

Abstract

High levels of expression of the p53 protein and gene mutations have been described in adult hepatocellular carcinomas. It has been postulated that specific mutations in exon 7 may be caused by aflatoxin exposure. To determine whether p53 mutations occur in childhood liver cancer unassociated with aflatoxin exposure or hepatitis B virus (HBV) infection, we have analyzed three histologically distinct tumor types. Two techniques were used to access p53 in the tumors: (1) expression studies of the p53 protein were performed using the polyclonal antibody CM1 and immunohistochemistry, and (2) DNA sequencing was performed. p53 Protein was detectable by immunohistochemistry in 10 of 15 hepatoblastomas, six of nine hepatocellular carcinomas, and one of one embryonal sarcomas. Solid phase single-stranded DNA sequencing across exons 5 through 9 showed normal sequence in all cases. These results indicate that p53 is overexpressed in a majority of childhood liver cancers, but this abnormal p53 expression does not seem to be caused by mutations in the p53 gene.