The mucus-hypersecreting tumor of the pancreas. Development and extension visualized by three-dimensional computerized mapping

Abstract

Background. Mucus‐hypersecreting tumor of the pancreas appears as dilated ducts and cystic spaces filled with mucus. To determine where such tumors arise and how they extend, computer‐aided three‐dimensional reconstruction was done of the ductal system. This also was used to visualize the spatial relationships among epithelial hyperplasia, dysplasia, and carcinoma in situ (CIS). Methods. Surgically removed pancreases were studied from 12 patients with mucus‐hypersecreting tumors. The specimens were fixed in buffered formaldehyde solution lo%, embedded in paraffin and semiserially sectioned at 3 pm at an interval of 60 pm. The ductal contours were diffentiated among ducts lined by ordinary epithelia, hyperplastic epithelia, dysplastic cells, or CIS and were inputted into a computer system that integrated a three‐dimensional image of ducts in the display. Results and Conclusions. (1) The tumors arose in the main pancreatic duct or its subbranches, and the cysts corresponded to segments expanded by the superficial growth of tumor cells; (2) areas of CIS arose in zones of preceding dysplasia, suggesting a dysplasia‐carcinoma sequence; and (3) dysplastic or cancerous cells often extended intraductally over the dilated segments of ducts.

A Population-Based, Descriptive Analysis of Malignant Intraductal Papillary Mucinous Neoplasms of the Pancreas

“…Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is a subtype that was first described in 1982, classified by the WHO in 1996, and not included in the International Classification of Diseases for Oncology (ICDO) until the ICDO, 3rd edition in 2000. IPMN lesions range in a spectrum from hyperplasia to adenoma to borderline neoplasm to carcinoma (7,8), representing another example of the well-described adenoma-carcinoma sequence (8)(9)(10)(11)(12). The clinical outcomes after diagnosis of malignant IPMN are poorly defined because of the relative rarity of this tumor type.…”

Clinicopathological significance of somatic RNF43 mutation and aberrant expression of ring finger protein 43 in intraductal papillary mucinous neoplasms of the pancreas

“…1 The dilated duct is lined with neoplastic epithelial cells exhibiting a papillary growth pattern with varying degrees of atypia and abundant mucin secretion; this appearance differs greatly from that of a conventional pancreatic cancer such as ductal adenocarcinoma that forms a highly invasive, firm mass. 2 However, intraductal papillary mucinous neoplasms often accompany or progress to ductal adenocarcinoma, resulting in a poor prognosis; therefore, intraductal papillary mucinous neoplasm is regarded as a precursor of ductal adenocarcinoma. 1 Currently, given the lack of appropriate biomarkers to monitor the disease phenotype, diagnosis and treatment of intraductal papillary mucinous neoplasms rely heavily on imaging studies in accordance with a guideline for the management of patients with these neoplasms, 3 thus indicating a pressing need to develop molecular markers on the basis of the molecular phenotypes.…”

Distinct progression pathways involving the dysfunction of DUSP6/MKP-3 in pancreatic intraepithelial neoplasia and intraductal papillary-mucinous neoplasms of the pancreas

“…22 Intraductal papillary-mucinous neoplasms are considered to be one of the precursor lesions of the pancreatic cancer, because some patients with intraductal papillary-mucinous neoplasms eventually develop an invasive papillary-mucinous carcinoma/invasive carcinoma associated with intraductal papillarymucinous neoplasm, which is comprised of either invasive colloid mucinous carcinoma or invasive ductal carcinoma. 23,24 Although there are some morphological similarities between the pancreatic intraepithelial neoplasia and intraductal papillarymucinous neoplasms, different clinicopathological features between them suggest that the pancreatic intraepithelial neoplasia and intraductal papillary-mucinous neoplasms would develop and progress through distinct pathways involving different genetic and molecular alterations, a hypothesis which seems to be endorsed by some molecular studies. [25][26][27] The aim of this study was to elucidate the roles of DUSP6 in the development and progression of pancreatic intraepithelial neoplasia and the intraductal papillary-mucinous neoplasm in association with other major tumor suppressive pathways.…”