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Updated: Jul 20, 2026

Comparative Lesions Analysis Through a Targeted Sequencing Approach
Published on: November 5, 2019
Accumulation of beta-catenin protein, mutations in exon-3 of the beta-catenin gene and a loss of heterozygosity of
Seong Min Kim1, Chuan Dong Sun, Ki Chung Park
1Department of Surgery, Yonsei University College of Medicine, Seoul, Korea, and Department of Hepatobiliary and Vascular Surgery, Medical School Hospital of Qingdao University, China.
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 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 SPT tissue suggest that these mutations are involved in SPT tumorigenesis.
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