在N-亚硝基-N-甲基脲诱导的大鼠肝肿瘤中，H-ras和K-ras基因不存在突变激活。
Mutational activation of H-ras and K-ras genes is absent in N-nitroso-N-methylurea-induced liver tumors in rats.
作者信息
Sakai H, Ogawa K
机构信息
Department of Pathology, Asahikawa Medical College.
出版信息
Jpn J Cancer Res. 1990 May;81(5):437-9. doi: 10.1111/j.1349-7006.1990.tb02587.x.
Abstract
We examined mutational activation of H- and K-ras genes in hyperplastic nodules and hepatocellular carcinomas induced by N-nitroso-N-methylurea or diethylnitrosamine using the polymerase chain reaction, followed by dot-blot hybridization. No mutational activation was detected in these hepatic lesions. The results indicate that low incidence of the activation of H- and K-ras genes in rat liver tumors is due to the organ specificity rather than the nature of the carcinogens used.
摘要
我们使用聚合酶链反应，随后进行斑点印迹杂交，检测了由N-亚硝基-N-甲基脲或二乙基亚硝胺诱导的增生性结节和肝细胞癌中H-和K-ras基因的突变激活情况。在这些肝脏病变中未检测到突变激活。结果表明，大鼠肝肿瘤中H-和K-ras基因激活的低发生率是由于器官特异性而非所用致癌物的性质。
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