Only wild-type c-Ki-ras codons 12, 13, and 61 in human pancreatic acinar cell carcinomas.

Activation of the c-Ki-ras proto-oncogene is more common in carcinomas of the pancreas than in other human carcinomas. Most such carcinomas are of the ductal cell phenotype. Ductal adenocarcinomas of the hamster pancreas have similar mutations, but acinar cell carcinomas of the mouse and rat pancreas lack the common c-Ki-ras mutations. Therefore, we examined 11 acinar cell carcinomas of the human pancreas for evidence of mutations at codons 12, 13, and 61. DNA was isolated from tumor cells in paraffin-embedded sections. The polymerase chain reaction was used to amplify the appropriate DNA sequence, and then allele-specific oligonucleotide hybridization and DNA sequence analysis were used to evaluate c-Ki-ras structure. Only wild-type sequences were found in codons 12, 13, and 61. Thus, in both the human and rodent species, mutations of c-Ki-ras appear to be more important in the genesis of ductal carcinomas than in the genesis of acinar cell carcinomas of the pancreas.