Clinicopathological Features

Intraductal spread of IDC is frequent in the well-differentiated type, common in the moderately differentiated type and occasional in the poorly differentiated type tumors [4, 24]. Some cases of well-differentiated tumors show marked intraductal extension, but none of the less-differentiated types show such marked intraductal extension. There is a significant correlation between the number of intraductal carcinoma foci and the grade of tumor differentiation [14].

IDC extends into the pancreatic tissue via stromal invasion. IDC also spreads through the pancreatic ductal tree. Intraductal spread is another important route of intrapancreatic extension in IDC. The intraductal carcinoma foci may be diffuse lesions involving the main pancreatic ducts, the large branch ducts and the small a

Fig. 5. Immunohistochemical features of IDC intraductal components. a The level of Ki67 immunoreactivity is low. b Most tumor cells show strong nuclear immunoreactivity for p53.

Fig. 5. Immunohistochemical features of IDC intraductal components. a The level of Ki67 immunoreactivity is low. b Most tumor cells show strong nuclear immunoreactivity for p53.

b a branch ducts, or they may occur focally in the pancreatic ducts. We observed the following distribution of intraductal carcinoma foci: 9.0% of foci were in the main pancreatic ducts, 64% in the large branch ducts and 27% in the small branch ducts [14]. The large branch ducts are the main routes of intraductal spread (fig. 7). The histogenesis of IDAP remains controversial. Duct cells, ductule cells and islets cells have been suggested as tumor progenitor cells [7, 25, 26]. The IDAP cells of the well-differentiated type are closely reminiscent of large interlobular duct cells [27]. Intraductal components of IDAP have a propensity to spread in large ducts rather than small branch ducts. These facts raise the possibility that IDAP might be derived from the epithelium of large branch ducts.

IDC can extend through the ducts beyond the tumor mass. The extension of the carcinoma as intraductal components has been cited as a particular problem in evaluating the surgical resection margin [24]. Intraductal carcinoma foci are observed even at the pancreatic resection margin. The intraductal carcinoma foci varied in location from the center (51%) or edge (35%) of the macroscopic tumor mass to outside the macroscopic tumor mass (14%). We reported that intraductal carcinoma foci were present outside the macroscopic tumor mass in 32% of IDAPs [14]. Intraductal spread of carcinoma is confined to the vicinity

Ki67 Index
Fig. 6. The Ki67 labeling index is significantly lower in the intraductal components than in the associated infiltrating components.
Fig. 7. Colonization along a large branch duct.

of the tumor mass in most cases [4]. The distance of intraductal carcinoma extension beyond the edge of the macroscopic tumor mass was limited to within 2.0 cm in our cases [14]. These findings emphasize that the pancreatic margin of resection should be at least 2.0 cm from the macroscopic tumor mass. In rare cases, the tumor may even spread along the main pancreatic duct into tumor-free

Fig. 8. IPMN showing a high papillary pattern.

tissue distant from the main tumor mass. None of the pancreatectomy specimens contained discontinuous foci of intraductal carcinoma [14, 24]. These facts suggest that multicentricity of ductal adenocarcinoma of pancreas occurs less frequently than was previously reported [24].

Ductal carcinoma of the pancreas is divided into two main categories: IDC and intraductal papillary mucinous neoplasm (IPMN) [4, 5]. IDC tends to invade extraductally from the early phase of its development. IPMT retains in situ or intraductal growth to a considerable extent before stromal invasion occurs [28]. Because of its poor prognosis, IDC should be differentiated from IPMN. Usually, this is not difficult because of the grossly solid and invasive tumor growth of IDC. There may occasionally be a problem distinguishing IDC with a marked intraductal extension from IPMN with clear invasion. In our study, three of 54 IDCs showed marked intraductal spread [14]. The intraductal components of these IDCs were confined in the immediate vicinity of associated infiltrating components. Moreover, intraductal components of IDC did not show a high papillary growth pattern, excessive secretion of mucin or association with the ade-nomatous components, which are characteristic of IPMN (fig. 8).

The presence or absence of intraductal components is not correlated with age, sex, tumor location, tumor size, or stage [14].

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