BACKGROUND AND AIM: K-ras oncogene is the most promising molecular marker of pancreatic cancer. However, the incidence of single and combined K-ras mutations in stool and pancreatic tissue is unknown, and it is not clear whether detection of the K-ras oncogene in stool could be employed in screening tests. PATIENTS/ METHODS: Stool and pancreatic tissue of patients with ductal adenocarcinoma (n = 36), cystadenocarcinoma (n = 1), periampullary carcinoma (n = 7), endocrine tumour (n = 2) and chronic pancreatitis (CP, n = 5) were analysed for mutated K-ras sequences prospectively. DNA of stool and pancreatic tissue was amplified by polymerase chain reaction and K-ras status was analysed by hybridisation. RESULTS: K-ras mutations were detected in the pancreatic tissue of 28 patients with ductal adenocarcinoma (78%), in 1 patient with cystadenocarcinoma, in 1 patient with periampullary carcinoma (14%) and in 1 patient with CP (20%). In 1 patient with an endocrine tumour, no K-ras mutations were diagnosed. K-ras mutations were detected in stool in 7 patients with ductal adenocarcinoma (20%), in 1 patient with cystadenocarcinoma and in 2 patients with CP (40%). Sensitivity of K-ras mutations for pancreatic cancer was 78% in tissue and 20% in stool. CONCLUSION: K-ras mutations lack specificity to discriminate malignant pancreatic disease from chronic inflammation in tissue and stool.
BACKGROUND AND AIM: K-ras oncogene is the most promising molecular marker of pancreatic cancer. However, the incidence of single and combined K-ras mutations in stool and pancreatic tissue is unknown, and it is not clear whether detection of the K-ras oncogene in stool could be employed in screening tests. PATIENTS/ METHODS: Stool and pancreatic tissue of patients with ductal adenocarcinoma (n = 36), cystadenocarcinoma (n = 1), periampullary carcinoma (n = 7), endocrine tumour (n = 2) and chronic pancreatitis (CP, n = 5) were analysed for mutated K-ras sequences prospectively. DNA of stool and pancreatic tissue was amplified by polymerase chain reaction and K-ras status was analysed by hybridisation. RESULTS:K-ras mutations were detected in the pancreatic tissue of 28 patients with ductal adenocarcinoma (78%), in 1 patient with cystadenocarcinoma, in 1 patient with periampullary carcinoma (14%) and in 1 patient with CP (20%). In 1 patient with an endocrine tumour, no K-ras mutations were diagnosed. K-ras mutations were detected in stool in 7 patients with ductal adenocarcinoma (20%), in 1 patient with cystadenocarcinoma and in 2 patients with CP (40%). Sensitivity of K-ras mutations for pancreatic cancer was 78% in tissue and 20% in stool. CONCLUSION:K-ras mutations lack specificity to discriminate malignant pancreatic disease from chronic inflammation in tissue and stool.
Authors: F Maire; S Micard; P Hammel; H Voitot; P Lévy; P-H Cugnenc; P Ruszniewski; P Laurent Puig Journal: Br J Cancer Date: 2002-08-27 Impact factor: 7.640