Imazeki F, Yokosuka O, Ohto M, Omata M
First Department of Medicine, Chiba University School of Medicine, Japan.
J Gastroenterol Hepatol. 1995 Nov-Dec;10(6):646-9. doi: 10.1111/j.1440-1746.1995.tb01364.x.
Recent studies have revealed that a point mutation at codon 249 in the p53 gene predominates in hepatocellular carcinoma (HCC) cases from Southern Africa and China, where infection with hepatitis B virus (HBV) and contamination of aflatoxin B1 in food are risk factors for HCC. This unique mutation from G to T at the third base in codon 249 observed in human HCC cases is suggested to be linked to aflatoxin exposure. Six ducks with HCC, five of which were fed a diet containing aflatoxin B1 for 1-2 years, were analysed for the presence of point mutations at this codon of the p53 gene by polymerase chain reaction and direct nucleotide sequencing. None of the six ducks with HCC showed the change at this codon regardless of duck hepatitis B virus infection. This suggests that aflatoxin B1 itself might not be involved in the unique mutation at codon 249 in hepatocarcinogenesis, or that other factors coincident with aflatoxin may be responsible for this unique mutation.
最近的研究表明,在南非和中国的肝细胞癌(HCC)病例中,p53基因第249密码子处的点突变占主导地位,在这些地区,乙型肝炎病毒(HBV)感染和食物中黄曲霉毒素B1污染是HCC的危险因素。在人类HCC病例中观察到的第249密码子第三个碱基由G突变为T这一独特突变,被认为与黄曲霉毒素暴露有关。对6只患有HCC的鸭子进行了分析,其中5只喂食含黄曲霉毒素B1的饲料1至2年,通过聚合酶链反应和直接核苷酸测序检测p53基因该密码子处的点突变情况。6只患有HCC的鸭子中,无论是否感染鸭乙型肝炎病毒,均未出现该密码子的变化。这表明黄曲霉毒素B1本身可能不参与肝癌发生过程中第249密码子处的独特突变,或者与黄曲霉毒素同时存在的其他因素可能是导致这一独特突变的原因。