Evaluation of c-K-ras in pancreatic carcinomas from Ela-1, SV40E transgenic mice

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.