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Accumulation of β‐catenin protein, mutations in exon‐3 of the β‐catenin gene and a loss of heterozygosity of 5q22 in solid pseudopapillary tumor of the pancreas
Author(s) -
Min Kim Seong,
Sun Chuan Dong,
Park Ki Chung,
Kim Ho Guen,
Lee Woo Jung,
Choi Seung Hoon
Publication year - 2006
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.20509
Subject(s) - loss of heterozygosity , exon , catenin , carcinogenesis , pancreas , biology , cancer research , chromosome , gene mutation , immunohistochemistry , microbiology and biotechnology , mutation , allele , genetics , gene , wnt signaling pathway , immunology , endocrinology
Background Solid pseudopapillary tumors (SPT) of the pancreas are neoplasms with a low malignant potential. The molecular events contributing to the pathogenesis of SPTs are still unknown. Objectives This study was intended to help better understand the early steps of human SPT development. Methods We microdissected 20 SPTs and normal pancreatic tissue. In addition, we examined the DNA from each SPT for mutations in exon‐3 of β‐catenin and loss of heterozygosity (LOH) on 9 chromosome arms using 10 microsatellite markers. Immunohistochemical staining for β‐catenin was performed. Results Activating mutations between codons 32 and 37 of β‐catenin exon‐3 were present in 16 cases (80%). Allelic loss on chromosome 5q22.1 was present in 10 cases (55.5%), while no allelic loss was found on chromosomes 1p, 6q, 9p, 9q, 11p, 11q, 17p, or 22q. Nuclear accumulation of β‐catenin was found in 20 cases (100%). Conclusion Mutations in exon‐3 of the β‐catenin gene, nuclear accumulation of β‐catenin, and LOH on chromosome 5q22.1 in SPT tissue suggest that these mutations are involved in SPT tumorigenesis. J. Surg. Oncol. 2006;94:418–425. © 2006 Wiley‐Liss, Inc.