首页> 外文期刊>Molecular Carcinogenesis >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.
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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.

机译:基于ras和p53基因的序列分析,ras基因突变激活可能不参与黄曲霉毒素B(1)诱导的人类肝癌发生的证据。

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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. Copyright 1999 Wiley-Liss, Inc.
机译:暴露于黄曲霉毒素B(1)(AFB(1))是发展为肝癌的危险因素之一。在大鼠中,ras基因的激活是AFB(1)诱导的肝癌发生中的普遍事件。尚不清楚人类是否发生过类似事件。通过分析p53基因的249位密码子,发现36例人类肝癌样本中有6例显示G→T反转,表明AFB(1)可能是肝癌发生的危险因素。然而,对ras家族基因的密码子12、13和61的分析显示,单个肿瘤中N-ras基因的61号密码子发生了A→T转换。显然,ras活化在人肝癌中很少见,AFB(1)可能不会诱导检测到的突变。这表明ras基因的激活可能不是AFB(1)相关的人类肝癌发生中的主要事件。版权所有1999 Wiley-Liss,Inc.

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