Abstract

Recently, a classification system for pancreatic intraepithelial neoplasia (PanIN) developed in 1999 was revised at a meeting of international experts on precursors of conventional pancreatic cancer. Many genetic alterations are shared by PanIN, invasive ductal carcinoma of the pancreas, and intraductal papillary-mucinous neoplasm including K-ras, p16, p53, and Smad4/DPC4 mutations. In this paper, genetic alterations in these tumors are discussed.

Copyright © 2007 S. Karger AG, Basel

Pancreatic cancer (PC) is a mostly fatal disease that is now thought to be a genetic disease. Therefore, various research on PC and its precursors has been done. Recently, intraductal lesions associated with PC were characterized at not only the histological but also the molecular level [1, 2]. Klimstra DS and Longnecker DS proposed to group them under the genetic term pancreatic intraductal neoplasia [3]. A classification system for PanIN developed in 1999 was recently revised at a meeting of international experts on precursors of PC [4, 5]. It has been established that the most likely precursor of conventional PC is the highgrade PanIN (PanIN-3). PanIN-3 lesions are found in 30-59% of pancreata harboring invasive ductal carcinomas (IDCs) of the pancreas [4-7], and many genetic alterations are shared by PanIN and IDS including K-ras, p16, p53, and Smad4/DPC4 mutations [5-9]. Moreover, these genetic alterations are also shared by intraductal papillary-mucinous neoplasms (IPMNs) [10]. In this section, genetic alterations in IPMN, PanIN, and IDC are discussed (tables 1, 2).

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