Evidence that mutational activation of the ras genes may not be involved in aflatoxin B(1)-induced human hepatocarcinogenesis, based on sequence analysis of the ras and p53 genes.
Exposure to aflatoxin B(1) (AFB(1)) is one of the risk factors for developing hepatoma. In rats, activation of the ras gene is a prevalent event in AFB(1)-induced hepatocarcinogenesis. It is not clear whether a similar event occurs in humans. By analysis of codon 249 of the p53 gene, six of 36 human hepatoma samples were found to show a G-->T transversion, suggesting that AFB(1) may be a risk factor for hepatocarcinogenesis. However, analysis at codons 12, 13, and 61 in the ras family genes revealed a A-->T transversion at codon 61 of the N-ras gene in a single tumor. Apparently, ras activation is rare in human hepatoma, and the mutation detected might not be induced by AFB(1). This suggests that activation of the ras gene may not be a major event in AFB(1)-related human hepatocarcinogenesis.
Chao
H K
HK
Department of Medical Research and Education, Veterans General Hospital-Taipei, Taipei, Taiwan, Republic of China.
Tsai
T F
TF
Lin
C S
CS
Su
T S
TS
D016604:Aflatoxin B1; D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced / Q000235:genetics*; D003062:Codon; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53; D011905:Genes, ras; D020022:Genetic Predisposition to Disease; D006801:Humans; D008113:Liver Neoplasms / Q000139:chemically induced / Q000235:genetics*; D009154:Mutation; D009693:Nucleic Acid Hybridization; D016133:Polymerase Chain Reaction; D051381:Rats; D017422:Sequence Analysis, DNA
D003062:Codon; D016604:Aflatoxin B1