Pancreatic carcinomas of acinar and mixed acinar/ductal phenotypes in Ela-1-myc transgenic mice do not contain c-K-ras mutations.

c-K-ras is activated by mutation at codon 12 in the majority of human pancreatic carcinomas of ductal but not acinar phenotype. The Ela-1-myc transgene when expressed in transgenic mice induces pancreatic carcinomas of both acinar and mixed acinar/ductal phenotype. The histopathology of 110 pancreatic carcinomas were characterized in this model. A high percentage of the low to moderately differentiated acinar cell carcinomas contain areas of ductal metaplasia. The latter tumors and several well-differentiated acinar tumors were evaluated for c-K-ras mutation to determine whether there is a relationship between the ductal phenotype and c-K-ras mutation. The polymerase chain reaction and allele-specific oligomer hybridization were used to determine whether the c-K-ras gene was mutated at codons 12, 13, or 61. Amplified DNA products from these tumors were also evaluated by single strand conformation polymorphism analysis. Only wild-type c-K-ras was found in these tissues. Not finding c-K-ras mutation in tumors containing ductal morphology indicates that c-K-ras mutation is not a required factor for acinar to ductal metaplasia or a factor in the tumorigenesis of pancreatic tumors that arise in acinar tissue.