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 u
sing the polymerase chain reaction and allele specific oligomer hybrid
ization 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 poly
morphism analysis. Only wild type c-K-ras was found in the tumors.