The five-year survival rate of CIS is almost 100%. However, it is not clear how many cases of CIS progress to invasive carcinoma. Actually, some CISs immediately progress to invasive carcinoma. In contrast, some CISs stay in the pancreatic duct for a long period and do not invade the pancreatic parenchyma.
CIS staying a long time in the pancreatic ducts will not necessarily lead to conventional PC acquiring a high malignant potentiality (fig. 3). Therefore, for an analysis of early features of conventional PC, small PCs with ICs are more suitable than CIS without invasion.
Whereas the PanIN classification excludes IPMN, the two tumor types are sometimes difficult to distinguish from each other . CIS-like IPMN is histologically similar to CIS, but its development is like that of IPMN; it spreads intraductally and hardly invades the pancreatic paremchyma (fig. 4). CIS-like IPMN should be also distinguished from precursors of conventional PC.
Both secondary ductal invasion and colonization of invasive carcinoma (cancerization of ducts) are treated as mimickers of PanIN-3 and are excluded for objective pancreatic lesions for PanIN . An infiltrating carcinoma in close proximity to a duct lesion and an abrupt transition from a highly atypical lesion to the normal duct epithelium both suggest the possibility of cancerization of the duct (fig. 5). In these cases, serial (step) sections may be helpful to
define the relationship between the duct lesion and the infiltrating carcinoma. However, it is often difficult to determine whether carcinoma initially spreads intraductally (CIS), or whether an infiltrating carcinoma secondarily involves the ducts (cancerization of ducts).
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