AIM:To investigate frequency and clinical significance of K-ras mutations in pancreatic diseases and to identify itsdiagnostic values in pancreatic carcinoma.METHODS:117 ductal lesions were identified in theavailable sections from pancreatic resection specimens ofpancreatic ductal adenocardnoma,comprising 24 pancreaticductal adenocarcinoma,19 peritumoral ductal atypicalhyperplasia,58 peritumoral ductal hyperplasia and 19 normalduct at the tumor free resection margin.24 ductal lesionswere got from 24 chronic pancreatitis.DNA was extracted.Codon 12 K-ras mutations were examined using the two-step polymerase chain reaction(PCR)combined withrestriction enzyme digestion,followed by nonradioisotopicsingle-strand conformation polymorphism(SSCP)analysisand by means of automated DNA sequencing.RESULTS:K-ras mutation rate of the pancreatic carcinomawas 79%(19/24)which was significantly higher than that inthe chronic pancreatitis 33%(8/24)(P<0.01).It was alsofound that K-ras mutation rate was progressively increasedfrom normal duct at the tumor free resection margin,peritumoralductal hyperplasia,peritumoral ductal atypical hyperplasia topancreatic ductal adenocarcinoma.The mutation pattern of K-ras 12 codon of chronic pancreatitis was GGT→GAT,GGT andCGT,which is identical to that in pancreatic carcinoma.CONCLUSION:K-ras mutation may play a role in the malignanttransformation of pancreatic ductal cell.K-ras mutation wasnot specific enough to diagnose pancreatic carcinoma. AIM: To investigate frequency and clinical significance of K-ras mutations in pancreatic diseases and to identify its diagnostic value in pancreatic carcinoma. METHODS: 117 ductal lesions were identified in the available sections from pancreatic resection specimens of pancreatic ductal adenocardnoma, comprising 24 pancreatic ductal adenocarcinoma, 19 peritumoral ductal atypicalhyperplasia, 58 peritumoral ductal hyperplasia and 19 normalduct at the tumor free resection margin. 24 ductal lesions were acquired from 24 chronic pancreatitis. DNA was extracted. Codon 12 K-ras mutations were examined using the two-step polymerase chain reaction (PCR) combined with restriction enzyme digestion, followed by nonradioisotopticingle-strand conformation polymorphism (SSCP) analysis and by means of automated DNA sequencing. RESULTS: K-ras mutation rate of the pancreatic carcinoma was 79% (19/24) which was significantly higher than that inthe chronic pancreatitis 33 % (8/24) (P <0.01) .It was alsofound that K-ras mutation rate was pro gressively increased from normal duct at the tumor free resection margin, peritumoral ductal hyperplasia, peritumoral ductal atypical hyperplasia topancreatic ductal adenocarcinoma. mutation pattern of K-ras 12 codon of chronic pancreatitis was GGT → GAT, GGT and CGT, which is identical to that in pancreatic carcinoma .CONCLUSION: K-ras mutation may play a role in the malignant transformation of pancreatic ductal cell. K-ras mutation was not specific enough to diagnose pancreatic carcinoma.