Murase T, Niwa K, Morishita S, Itoh N, Mori H, Tanaka T, Tamaya T
Department of Obstetrics and Gynecology, Gifu University School of Medicine, Japan.
Cancer Lett. 1995 Jun 8;92(2):223-7. doi: 10.1016/0304-3835(95)03782-r.
To examine K-, H-, or N-ras and p53 gene mutations in mouse endometrial carcinogenesis induced by N-methyl-N-nitrosourea and 17 beta-estradiol, we performed polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) in 13 adenocarcinomas and 11 other preneoplastic lesions. A significant shifted band in exon 5 of p53 using PCR-SSCP was detected in one of 13 adenocarcinomas. Direct sequencing showed that the mutation was TCA-to-TGA (Ser-to-End) transition. These results suggest that ras gene mutations were not related to carcinogenesis and inactivation of p53 may occur with low frequency during the mouse endometrial carcinogenesis in this model.
为检测由N-甲基-N-亚硝基脲和17β-雌二醇诱导的小鼠子宫内膜癌发生过程中K-、H-或N-ras以及p53基因突变情况,我们对13例腺癌和11例其他癌前病变进行了聚合酶链反应-单链构象多态性分析(PCR-SSCP)。在13例腺癌中的1例中,利用PCR-SSCP在p53基因第5外显子检测到一条明显迁移的条带。直接测序显示该突变是TCA到TGA(丝氨酸到终止密码子)的转变。这些结果表明,在该模型的小鼠子宫内膜癌发生过程中,ras基因突变与致癌作用无关,p53基因失活可能以低频率发生。