ONLY WILD-TYPE C-KI-RAS CODON-12, CODON-13, AND CODON-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 hamste r pancreas have similar mutations, but acinar cell carcinomas of the m ouse and rat pancreas lack the common c-Ki-ras mutations. Therefore, w e examined 11 acinar cell carcinomas of the human pancreas for evidenc e of mutations at codons 12, 13, and 61. DNA was isolated from tumor c ells 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 co dons 12, 13, and 61. Thus, in both the human and rodent species, mutat ions 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 pancre as. (C) 1994 Wiley-Liss, Inc.