Kuhlmann E, Terhune P G, Longnecker D S
Department of Pathology, Dartmouth Medical School, Lebanon, NH 03756.
Carcinogenesis. 1993 Dec;14(12):2649-51. doi: 10.1093/carcin/14.12.2649.
c-K-ras is activated by mutation at codon 12 in the majority of human pancreatic carcinomas of ductal, but not acinar, phenotype. Therefore, evaluation of c-K-ras in experimentally induced pancreatic carcinomas in animal models is of interest for comparison with the human disease. Acinar cell carcinomas and islet cell tumors arising in two strains of transgenic mice carrying the Ela-1-SV40E transgene were evaluated using the polymerase chain reaction and allele specific oligomer hybridization to seek evidence of c-K-ras mutation at codons 12, 13 and 61. Amplified DNA products, including codons 12 and 13, from the majority of these tumors were also evaluated by single strand conformation polymorphism analysis. Only wild type c-K-ras was found in the tumors.
在大多数具有导管表型而非腺泡表型的人胰腺癌中,c-K-ras在第12密码子处因突变而被激活。因此,在动物模型中对实验性诱导的胰腺癌进行c-K-ras评估,对于与人类疾病进行比较很有意义。使用聚合酶链反应和等位基因特异性寡聚物杂交技术,对携带Ela-1-SV40E转基因的两株转基因小鼠中出现的腺泡细胞癌和胰岛细胞瘤进行评估,以寻找c-K-ras在第12、13和61密码子处发生突变的证据。这些肿瘤中的大多数扩增DNA产物(包括第12和13密码子)也通过单链构象多态性分析进行了评估。在这些肿瘤中仅发现野生型c-K-ras。