Seung Hoon Choi

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.

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