Accumulation of beta-catenin protein, mutations in exon-3 of the beta-catenin gene and a loss of heterozygosity of 5q22 in solid pseudopapillary tumor of the pancreas |
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Authors: | Min Kim Seong Sun Chuan Dong Park Ki Chung Kim Ho Guen Lee Woo Jung Choi Seung Hoon |
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Affiliation: | Department of Surgery, Yonsei University College of Medicine, Seoul, Korea, and Department of Hepatobiliary and Vascular Surgery, Medical School Hospital of Qingdao University, China. |
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Abstract: | 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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Keywords: | solid pseudopapillary tumor pancreas mutation immunohistochemistry loss of heterozygosity |
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