QMSP could accurately distinguish patients with pancreatic cancer and other periampullary cancers from those with benign periampullary disease; 73.2% of patients with pancreatic ductal adenocarcinoma had at least 1 gene positive for methylation by QMSP (defined as > or =1% TFPI-2 DNA and > or =3% methylated NPTX2 and Cyclin D2 DNA) in their brush samples, compared with 80% of patients with a biliary tract cancer and only 13.6% of patients with a benign stricture (P < .001).
We thus conclude that epigenetic inactivation of TFPI-2 is a common mechanism that contributes to the aggressive phenotype of pancreatic ductal adenocarcinoma.