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Non‐cystic solid‐pseudopapillary tumor of the pancreas showing nuclear accumulation and activating gene mutation of β‐catenin
Author(s) -
Nishimori Isao,
Kohsaki Takuhiro,
Tochika Naoshige,
Takeuchi Tamotsu,
Minakuchi Tomoko,
Okabayashi Takehiro,
Kobayashi Michiya,
Hanazaki Kazuhiro,
Onishi Saburo
Publication year - 2006
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2006.02034.x
Subject(s) - pancreas , catenin , carcinogenesis , pathology , biology , phenotype , wnt signaling pathway , exon , cancer research , gene , medicine , genetics , endocrinology
Solid‐pseudopapillary tumor (SPT) is an unusual pancreatic neoplasm that is characterized by a mixture of solid and cystic components and a fibrous capsule. Recently, the tumorigenesis of SPT has been reported to be associated with gene mutations of β‐catenin, which is a molecule participating in the Wnt signaling pathway. Reported herein is the case of a 53‐year‐old woman with SPT. The tumor, approximately 3 cm in diameter in the pancreas body, had a clear margin and central calcification but had neither a cystic component nor fibrous capsule. Several lines of pathological findings in the surgically resected specimen indicated SPT: (i) pseudopapillary proliferation of eosinophilic polygonal cells with oval nuclei; (ii) positive expression of several marker molecules indicating differentiation into acinar and endocrine cells; and (iii) zymogen granule‐like structures in the cytoplasm on electron microscopy. Further, the tumor cells had intense nuclear accumulation of β‐catenin and an activating mutation, 34 Gly(GGA) to Arg(AGA), in exon 3 of the β‐catenin gene, as previously reported in most SPT. These findings suggest that association of the β‐catenin phenotype with development of the rare phenotype of SPT, a non‐cystic and unencapsulated tumor, is unlikely.