Yuasa Y, Reddy E P, Rhim J S, Tronick S R, Aaronson S A
Jpn J Cancer Res. 1986 Jul;77(7):639-47.
An N-ras transforming gene was detected in human rectal carcinoma-derived cells (7060) and molecularly cloned. The genetic lesion responsible for the transforming activity of the 7060 oncogene was localized to a single nucleotide transition from A to T in codon 61 of the predicted protein. This lesion in the second exon results in substitution of histidine for glutamine at this position. We also found an EcoRI restriction fragment length polymorphism, consisting of two alleles, of the human c-myb gene. The 7060-transformed epithelial cells showed the homozygous phenotype, while normal fibroblasts of the same patient showed the heterozygous phenotype. This suggests a relationship between the phenotypic change in the c-myb locus and the induction of the 7060 tumor.
在人直肠癌衍生细胞（7060）中检测到一个N-ras转化基因并进行了分子克隆。导致7060癌基因转化活性的遗传损伤定位于预测蛋白第61密码子处从A到T的单个核苷酸转换。第二个外显子中的这种损伤导致该位置的谷氨酰胺被组氨酸取代。我们还发现了人类c-myb基因的一种EcoRI限制性片段长度多态性，由两个等位基因组成。7060转化的上皮细胞表现出纯合表型，而同一患者的正常成纤维细胞表现出杂合表型。这表明c-myb基因座的表型变化与7060肿瘤的诱导之间存在关联。
