Pancreatic Ductal Adenocarcinomas with Multiple Large Cystic Structures: A Clinicopathologic and Immunohistochemical Study of Seven Cases
Takeo Nitta, Tomoko Mitsuhashi, Yutaka Hatanaka, Satoshi Hirano, Yoshihiro Matsuno. Hokkaido University Hospital, Sapporo, Hokkaido, Japan; Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan
Background: Pancreatic ductal adenocarcinoma (PDA) with cystic change may be confused with other cystic neoplasms of the pancreas, and must therefore be included in the differential diagnosis. Those tumors do not constitute a uniform group, and are classified into several types according to the features of the cysts.
Design: A total of 200 surgically resected PDAs were examined for the present analysis. Among them, 22 (11%) showed cystic lesions. Fifteen out of these 22 cases were classifiable as cystic PDAs by the previously reported criteria (ref. Kosmahl et al, 2005 and Adsay, et al, 2011). The remaining 7 cases were PDAs with a multiple large cystic (MLC) structure not classifiable by those criteria. Histological and immunohistochemical studies were performed using formalin-fixed, paraffin-embedded (FFPE) tissue. In the 7 PDAs with MLC structures, the KRAS oncogene mutation in codon 12 was studied. Follow-up information after surgical resection was available for all 22 patients. The mean follow-up period was 23 months (range, 4-60 months). Postoperative survival of patients with cystic PDA, with and without a MLC structure, were compared.
Results: PDAs with MLC were associated with more than 5 large cystic structures and numerous intratumoral microcysts, lined by epithelial cells with various degrees of atypia. The maximal cyst diameter (average 3.7 cm) was much larger than that of previously reported. Immunohistochemically, the tumor cells and cyst-lining epithelia were negative for mucin core protein (MUC) 1, MUC2, and MUC6, and showed only focal staining for MUC5AC. Maspin, CEA, and p53 were strongly positive, and the Ki-67 labeling index was high in both tumor cells and cyst-lining epithelia. KRAS oncogene mutation was identified in 6 of the 7 cases. Postoperative outcome in the MLC lesion group did not appear to differ significantly from cases without such lesions.
Conclusions: The MLC structures in PDA might be a mixture of ectatic neoplastic glands and retention cysts with ductal cancerization or pancreatic intraepithelial neoplasia; however, they might represent a new entity of cystic PDA because of the unusually large size of the dilated cysts. Diagnostic pathologists should bear in mind that MLC-type PDA can form cystic lesions similar to those of intraductal papillary neoplasms or mucinous cystic neoplasms.
Wednesday, March 6, 2013 1:00 PM
Poster Session VI # 132, Wednesday Afternoon