PMC4727070_01
(A) Coronal section of a computed tomography scan revealing an irregular mass (arrow) in the pancreatic head exhibiting lower enhancement relative to the non-tumor pancreatic parenchyma in the arterial-dominant phase. Cysts located in the inferior part of the irregular mass were observed. (B) Magnetic resonance cholangiopancreatography showing stenosis of the main pancreatic and common bile ducts, caused by the mass-neighboring cysts.
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A coronal section revealed the presence of cysts in the inferior part of the mass, and main pancreatic duct distension by ~11 mm (Fig. 1A). Magnetic resonance cholangiopancreatography revealed stenosis of the main pancreatic and common bile ducts, caused by the mass-neighboring cysts (Fig. 1B).
Serial sections of the pancreatic tumors. The IPMN-involved ducts appear dilated and the cut surface of the invasive tumor (arrow) is solid and whitish yellow. IPMN, intraductal papillary mucinous neoplasm.
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Macroscopically, the cut surface of the invasive tumor was solid and whitish yellow, measuring 19 mm in diameter (Fig. 2).
Hematoxylin and eosin-stained sections of the tumor. (A) The arrows indicate the invasive carcinoma. Irregularly dilated abnormal ducts involved by the intraductal papillary mucinous neoplasm (IPMN) may be seen in and beneath the invasive cancer component; magnification, x1. (B) Area of the open square shown in (A); magnification, x10. The arrows indicate the main pancreatic duct involved by the IPMN. (C) Area of the open square shown in (B); magnification, x40. Photomicrograph of the intestinal-type IPMN with high-grade dysplasia. Part of the IPMN was budding and intruding into the surrounding anaplastic lesion (arrow). (D) Area of the open square shown in (C); magnification, x100. The IPMN cells exhibited continuous transition to invasive anaplastic carcinoma. The arrow indicates bizarre-appearing giant cells.
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The histopathological and immunohistochemical findings are summarized in Figs. 3 and 4, respectively. As shown in Fig. 3A and B, the focus of the invasive carcinoma was located at the periphery of the IPMN. However, a part of the IPMN with high-grade dysplasia exhibited continuous transition to invasive carcinoma, lacked polarity, and displayed stratified and pleomorphic nuclei (Fig. 3C); these lesions had an MIB-1 index of ~80%.
Immunohistochemical analysis of the pancreatic tumor. (A) The intraductal papillary mucinous neoplasm (IPMN) cells exhibited mucin 2 immunoreactivity. (B) The mononuclear and multinuclear cells of the anaplastic carcinoma (ACP) exhibited immunoreactivity for cytokeratin 7. (C) A higher mindbomb E3 ubiquitin protein ligase 1 labeling ratio was observed in the IPMN with high-grade dysplasia compared with the ACP (asterisk).
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The histopathological and immunohistochemical findings are summarized in Figs. 3 and 4, respectively. The IPMN cells exhibited mucin 2 immunoreactivity (anti-MUC2 monoclonal mouse antibody; dilution, 1:20; cat. no., 555926; BD Biosciences) (Fig. 4A). The mono- and multinuclear cells of the ACP exhibited similar immunoprofiles (monoclonal mouse antibody against cytokeratin 7; dilution, 1:100; cat. no., M7014; Dako) (Fig. 4B). The mindbomb E3 ubiquitin protein ligase 1 (MIB-1; Ki-67) mean labeling index was ~5% around the IPMN (Fig. 4C), and ~25% in sites distant from the IPMN (MIB-1 monoclonal mouse antibody; dilution, 1:150; cat. no., M7240; Dako).