RAS ONCOGENE MUTATIONS IN TETRAFLUOROETHYLENE LIVER

工作总结：H-ras密码子61突变的低频率(155，9/59) 在肝细胞肿瘤中被检测到，与更高的 自发的频率(本研究的59%和历史数据的56%) 肝脏肿瘤。在突变频率或 暴露组之间或良性与恶性之间的光谱 肝细胞肿瘤。密码子12、13和61的K-ras突变 在肝细胞癌中未检测到H-ras基因117位密码子突变 新的电浆。频率与在肝脏中发现的频率相似 结构上相关的化学物质四氯乙烯产生的肿瘤 (Tce)。这些数据表明，FGE诱导的肝细胞肿瘤和 结构上最相关的化学类的新肿瘤和肿瘤 可能通过依赖H-和K-ras原癌基因的途径发生 激活。手稿正在准备中。

Summary of Work: A low frequency (155, 9/59) of H-ras codon 61 mutations was detected in hepatocellular neoplasms when compared to the higher frequency (59% of this study and 56% of historical data) in spontaneous liver neoplasms. There was no difference in the mutation frequency or spectrum among exposure groups or between benign and malignant heopatocellular neoplasms. K-ras mutations at codons as 12, 13, and 61 and H-ras mutations at codon 117 were not detected in hepatocellular newplasms. The frequency to be similar to those identified in liver neoplasms from the structurally related chemical tetrachloroethylene (TCE). These data suggest that FGE-induced heptocellular neoplasms and newplasms and neoplasms from structurally related chemical classes most likely develop by pathway ndependent of H- and K-ras proto-oncogene activation. The manuscript is in preparation.