Maheshwari K K, Parsa I, Marsh W H
Medical University of South Carolina, Department of Pediatrics, Charleston 29425.
Biochem Int. 1990;20(1):117-25.
Point mutation and activation of c-Ha-ras oncogene was studied at various stages of carcinogenesis in cell lines developed from MNU-treated human pancreas explants. DNAs from normal pancreas and nontumorigenic cell lines showed no transforming activity in NIH 3T3 cells whereas DNA from one of the tumorigenic cell lines transformed NIH 3T3 cells. In this cell line the point mutation was demonstrated to be at codon 12 of c-Ha-ras gene by the loss of an Msp I site. The mutation possibly affected the transcription of c-Ha-ras gene which in turn contributed to the transformation of these cells.
在由N-甲基-N-亚硝基脲（MNU）处理的人胰腺外植体所形成的细胞系的致癌作用的各个阶段，研究了c-Ha-ras癌基因的点突变和激活情况。来自正常胰腺和非致瘤性细胞系的DNA在NIH 3T3细胞中未显示转化活性，而来自其中一个致瘤性细胞系的DNA可转化NIH 3T3细胞。在该细胞系中，通过Msp I位点的缺失证明c-Ha-ras基因的第12密码子存在点突变。该突变可能影响了c-Ha-ras基因的转录，进而促成了这些细胞的转化。
