Patients with long-standing chronic pancreatitis are thought to be at increased risk of
developing pancreatic ductal adenocarcinoma, but the mechanism for this increased risk is
unknown. Since increasing evidence supports the notion that infiltrating pancreatic ductal
adenocarcinomas arise from pancreatic intraepithelial lesions (PanINs), we sought to
determine if patients with chronic pancreatitis harbor PanINs with alterations in tumor
suppressor genes that are associated with infiltrating pancreatic ductal adenocarcinoma. We …