Abstract
To determine whether intraductal papillary mucinous neoplasms of the pancreas (IPMNs) have a different genetic background compared with ductal adenocarcinoma (PDAC). The biologic and clinical behavior of IPMNs and IPMN-associated adenocarcinomas is different from PDAC in having a less aggressive tumor growth and significantly improved survival. Up to date, the molecular mechanisms underlying the clinical behavior of IPMNs are incompletely understood. 128 cystic pancreatic lesions were prospectively identified during the course of 2 years. From the corresponding surgical specimens, 57 IPMNs were separated and subdivided by histologic criteria into those with low-grade dysplasia, moderate dysplasia, high-grade dysplasia, and invasive cancer. Twenty specimens were suitable for DNA isolation and subsequent performance of array CGH. While none of the IPMNs with low-grade dysplasia displayed detectable chromosomal aberrations, IPMNs with moderate and high-grade dysplasia showed frequent copy number alterations. Commonly lost regions were located on chromosome 5q, 6q, 10q, 11q, 13q, 18q, and 22q. The incidence of loss of chromosome 5q, 6q, and 11q was significantly higher in IPMNs with high-grade dysplasia or invasion compared with PDAC. Ten of 13 IPMNs with moderate dysplasia or malignancy had loss of part or all of chromosome 6q, with a minimal deleted region between linear positions 78.0 and 130.0. This study is the first to use array CGH to characterize IPMNs. Recurrent cytogenetic alterations were identified and were different than those described in PDAC. Array CGH may help distinguish between these 2 entities and give insight into the differences in their biology and prognosis.
Highlights
This study is the first to use array CGH to characterize intraductal papillary mucinous neoplasms of the pancreas (IPMNs)
Compared with ductal adenocarcinoma of the pancreas, IPMNs are characterized in having a less aggressive biologic and clinical behavior, with survival rates of more than 60% even for invasive carcinoma associated with IPMN after surgical removal.[1]
IPMNs may demonstrate a spectrum of cytologic atypia ranging from mucinous epithelium with minimal cytologic atypia to frank invasive adenocarcinoma[7] not infrequently in different areas of the same surgical specimen.[12,13,14]
Summary
128 cystic pancreatic lesions were prospectively identified during the course of 2 years. Tissue samples from surgical specimens were collected and stored fresh frozen at the pancreatic tumor bank of the Massachusetts General Hospital, Boston, Massachusetts. From these specimens, 57 IPMN samples were evaluated by histology and 20 were suitable for DNA isolation. For tumors of mixed type, which component (main duct or branch duct) was used for DNA extraction is known from gross descriptions of the resection specimen, and this is indicated in Supplemental Table 1 (see Table, Supplemental Digital Content 1, http://links.lww.com/A790). In addition to the described 20 samples deriving from 20 different patients, we analyzed DNA from a second anatomic location for patient #10 (specimen #10a with moderate dysplasia and #10b with high-grade dysplasia).
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