Most pancreatic neoplasms arise from histologically recognizable precursors. The 3 most common precursors to invasive cancer - pancreatic intraepithelial neoplasias, mucinous cystic neoplasms, and intraductal papillary mucinous neoplasms - all contain tall columnar mucin-producing cells. In PabIn lesions, these cells line small native pancreatic ductules; in IPMNs, they form a viliform mass within large native pancreatic ducts. In contrast, MCNs contain de novo cysts not connected to the native pancreatic duct system. The recognition of incipient neoplasia in the pancreas is important, because it provides opportunity to identify a curable disease. For example, the complete removal of a mucinous cystadenoma can cure a patient of a neoplasm that, if not removed, can progress to an incurable infiltrating cancer. Similarly, the application of modern molecular screening tests has the potential to lead to the identification of early-stage, and therefore surgically treatable, ductal adenocarcinomas and their precursors. Molecular biology may lead not only to the earlier diagnosis of pancreatic tumors but also to the more accurate diagnosis of these neoplasms. The molecular characterization of pancreaticoblastomas, acinar cell carcinomas, and solid-pseudopapillary neoplasms has revealed that there are seperate genetic pathways of neoplastic progression for pancreatic ductal and nonductal neoplasms. Genetic changes may, in conjunction with histologic study, provide important information on tumor type and thus on patient treatment and prognosis.
|Original language||English (US)|
|Number of pages||8|
|Journal||Current Problems in Cancer|
|State||Published - Jul 1 2002|
ASJC Scopus subject areas
- Cancer Research