期刊
JOURNAL OF SURGICAL ONCOLOGY
卷 94, 期 5, 页码 418-425出版社
WILEY-BLACKWELL
DOI: 10.1002/jso.20509
关键词
solid pseudopapillary tumor; pancreas; mutation; immunohistochemistry; loss of heterozygosity
Background: Solid pseudopapillary tumors (SPIT) of the pancreas are neoplasms with a low malignant potential. The molecular events contributing to the pathogenesis of SPITS are still unknown. Objectives: This study was intended to help better understand the early steps of human SPIT 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 beta-catenin and loss of heterozygosity (LOH) on 9 chromosome arms using 10 microsatellite markers. Immunohistochemical staining for beta-catenin was performed. Results: Activating mutations between codons 32 and 37 of beta-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 beta-catenin was found in 20 cases (100%). Conclusion: Mutations in exon-3 of the beta-catenin gene, nuclear accumulation of beta-catenin, and LOH on chromosome 5q22.1 in SPIT tissue suggest that these mutations are involved in SPT tumorigenesis.
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