Newcomb E W, Diamond L E, Sloan S R, Corominas M, Guerrerro I, Pellicer A
Department of Pathology, New York University Medical Center, NY 10016.
Environ Health Perspect. 1989 May;81:33-7. doi: 10.1289/ehp.898133.
A survey of a large series of radiation- or chemically induced thymic lymphomas in (AKR X RF)F1, RF/J, 129/J, and C57BL/6J mouse strains for activated ras oncogenes showed that of the tumors containing transforming activity, in more than 75% of the cases this activity segregated with either K-ras or the N-ras gene. H-ras activity was never detected. The genetic background of the host influenced susceptibility to tumor induction and oncogene activation. The K-ras gene was preferentially activated over the N-ras gene (approximately 2:1) whether the inducing agent was radiation or the chemical N-nitrosomethylurea. The activating mutation for the K-ras gene was consistently identified as a GGT to GAT transition in codon 12. In contrast, several different mutations of the N-ras gene were identified and localized to codons 12, 13, or 61. Assessment of the allelic composition of the ras locus shows that some proportion of the tumors lost the normal ras allele.
对（AKR×RF）F1、RF/J、129/J和C57BL/6J小鼠品系中大量辐射或化学诱导的胸腺淋巴瘤进行的一项关于活化ras癌基因的调查显示，在具有转化活性的肿瘤中，超过75%的情况下，这种活性与K-ras或N-ras基因相关。从未检测到H-ras活性。宿主的遗传背景影响肿瘤诱导和癌基因激活的易感性。无论诱导剂是辐射还是化学物质N-亚硝基甲基脲，K-ras基因比N-ras基因更易被优先激活（约为2:1）。K-ras基因的激活突变一直被确定为密码子12处的GGT到GAT转换。相比之下，鉴定出了N-ras基因的几种不同突变，并定位到密码子12、13或61。对ras基因座等位基因组成的评估表明，一定比例的肿瘤失去了正常的ras等位基因。
