Kijima H, Abe Y, Yamazaki H, Ohnishi Y, Ueyama Y, Tamaoki N, Nakamura M
Department of Pathology, Tokai University School of Medicine, Kanagawa, Japan.
Anticancer Res. 1994 Nov-Dec;14(6B):2583-7.
We examined the Ki-ras oncogene point mutation in primary tumors and tumor xenografts as a marker of genetic stability. We detected point mutations at codon 12 of the Ki-ras oncogene in 21.3% (17/80) of the tumor xenografts as well as 21.0% (17/81) of the primary human neoplasms. The mutation from GGT (glycine) to GAT (aspartic acid) was the most frequent mutation in the tumor xenografts (64.7%, 11/17) as well as in the primary human neoplasms (64.7%, 11/17). The point mutation at codon 12 of the Ki-ras gene showed no discrepancy between the original human neoplasms and their xenografts in all 19 cases. The findings suggested that the point mutation at codon 12 of the Ki-ras gene was very stable in human neoplasms and their tumor xenografts through serial transplantation.
我们检测了原发性肿瘤和肿瘤异种移植中Ki-ras癌基因的点突变,以此作为遗传稳定性的一个标志物。我们在21.3%(17/80)的肿瘤异种移植以及21.0%(17/81)的原发性人类肿瘤中检测到了Ki-ras癌基因第12密码子的点突变。从GGT(甘氨酸)到GAT(天冬氨酸)的突变是肿瘤异种移植(64.7%,11/17)以及原发性人类肿瘤(64.7%,11/17)中最常见的突变。在所有19例病例中,Ki-ras基因第12密码子的点突变在原发性人类肿瘤及其异种移植之间未显示出差异。这些发现表明,通过连续传代移植,Ki-ras基因第12密码子的点突变在人类肿瘤及其肿瘤异种移植中非常稳定。