Genetic Alteration in IPMN

IPMNs of the pancreas constitute a unique clinicopathological entity with an overall incidence of associated invasive malignancy of 20%. Loss of p16 and DPC4/Smad4 expression occur more frequently in intraductal papillary-mucinous carcinoma, or with associated invasive carcinoma, compared with adenoma/borderline IPMN. Aberrant protein expression of cell cycle regulatory genes p16, p21, p27, cycline D1, pRb, and p53 of IPMN in their development is similar to that of PanIN in the current progression model of PC, and may also represent the subsequent risk of invasive carcinoma [10]. In Japan, invasive carcinoma derived from IPMN was classified in the 5th edition of the general rules for the study of PC (in Japanese) and the first English edition of the classification of PC by the Japan Pancreas Society [18, 19]. Invasive carcinoma derived from IPMN with extrapancreatic expansion should be treated as conventional IDC because of its aggressive biological behavior. Some IPMNs are thought to progress to invasive carcinoma through different pathways from that of IDC [20]. The prognosis of invasive carcinoma derived from IPMN is still controversial, i.e. the prognosis in patients with invasive carcinoma derived from IPMN is thought to be as poor as in patients with conventional IDC [21], although it is also thought to be more favorable than in patients with conventional IDC [22].

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