Clinical Articles
Copyright ©The Author(s) 1996. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 1996; 2(3): 161-164
Published online Sep 15, 1996. doi: 10.3748/wjg.v2.i3.161
Overexpression and mutations of tumor suppressor gene p53 in hepatocellular carcinoma
Dong Wang, Jing-Quan Shi
Dong Wang, Jing-Quan Shi, Department of Pathology, Third Military Medical College, Chongqing 630042, China
Dong Wang, MD, Associate Professor and Director of the Department of Clinical Pathology, Daping Hospital, having published 19 papers and one book.
Author contributions: All authors contributed equally to the work
Correspondence to: Dong Wang, MD, Associate Professor, Director, Department of Pathology, Third Military Medical College, Chongqing 630042, China
Received: June 16, 1996
Revised: July 15, 1996
Accepted: August 13, 1996
Published online: September 15, 1996

AIM: To examine the prevalence of p53 mutations in cases of hepatocellular carcinoma (HCC) in the Chongqing area of China, and the relationship between p53 mutations and the clinicopathological features of HCC, as well as its risk factors.

METHODS: The overexpression and point mutations of tumor suppressor gene p53 in 38 cases of HCC were detected by a sensitive antigen retrieval fluid (ARF) immunohistochemical method, polymerase chain reaction (PCR) a2 restriction fragment length polymorphism (RFLP) analysis, and a single strand conformation polymorphism (SSCP) a2silver staining analysis.

RESULTS: The results showed that 16 of 38 HCCs were positive for P53 protein (42.1%). Seven HCCs (18.4%) had a p53 mutation at codon 249, and 2 other HCCs had point a mutation within exon 7 but not at codon 249. Among 9 cases of HCC which showed genetic mutations, 8 cases (88.9%) were positive for p53 protein. Both p53 overexpression and mutation were significantly related to the degree of HCC tissue differentiation and the presence or absence of metastases. The frequency of p53 mutations was consistent with the high prevalence of HBV infection and moderate aflatoxin B1 (AFB1) exposure in the Chongqing area.

CONCLUSION: Our results suggest that AFB1 acts synergistically with HBV in the generation of p53 mutations. Furthermore, dietary exposure to AFB1 may mainly contribute to the tumor specific mutation at codon 249, while HBV may account for other scattered mutations found in cases of HCC.

Keywords: Liver neoplasms, Genes, Suppressor, Tumor protein p53 point mutation