Pancreatic intraepithelial neoplasia (PanIN) is a progression model of invasive ductal carcinoma (IDC) of the pancreas concerning genetic alterations, and its adoption requires conditions of invisible ductal lesions without obvious duct dilation. Intraductal components (ICs) of conventional pancreatic cancer (PC) are thought to include intraductal spread of carcinoma in situ (CIS) and intraductal extension of IDC (cancerization of ducts: ductal invasion and colonization). CIS is usually low papillary or flat, and its histology changes to tubular adenocarcinoma with desmoplasia in the case of invasion. The invasive component shows more enlarged individual tumor cells and more atypia than IC. Most conventional PCs are found with various diagnostic imaging techniques by direct or indirect findings of the main pancreatic duct such as stenosis, interruption, or secondary dilation of the main pancreatic duct. PC is a mostly fatal disease that requires new treatment. In order to improve the poor prognosis associated with this disease, we must detect small PCs at a curable stage and recognize the precursors of PC.
Copyright © 2007 S. Karger AG, Basel
The change from a normal to a cancer cell is caused by accumulation of genetic alterations. Specific genetic alterations are thought to be associated with each progression step. Since tumors associated with oncogenes and tumor suppressor genes were discovered, cancer has also been thought of a genetic disease. Lesions with the ability to progress to cancer by accumulating genetic alterations can be called precursors of cancer.
Most pancreatic cancers (PCs) that are diagnosed and treated are conventional PCs with poor prognosis. To improve this very poor prognosis, we must clarify the risk factors of PC. It is especially important to know what kinds of lesion progress to PC, i.e. to clarify the characteristics of PC precursors.
In this section, intraductal lesions that were thought to be precursors of conventional PC and related molecular findings are discussed.
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