Wang P, Fromowitz F, Koslow M, Hagag N, Johnson B, Viola M
Department of Medicine, State University of New York, Stony Brook 11794.
Br J Cancer. 1991 Sep;64(3):531-3. doi: 10.1038/bjc.1991.344.
We used RNAase protection and restriction fragment length polymorphism assays to detect activating mutations of c-src in a spectrum of human tumours. No mutations were detected at codons 98, 381, 444, and 530. We conclude that mutational activation is not the mechanism of enhancement of pp60c-src-specific kinase activity found in a number of human cancer types.
我们使用核糖核酸酶保护法和限制性片段长度多态性分析来检测一系列人类肿瘤中c-src的激活突变。在密码子98、381、444和530处未检测到突变。我们得出结论,突变激活不是在多种人类癌症类型中发现的pp60c-src特异性激酶活性增强的机制。