[Detection of alterations of the DPC4 gene in paraffin-embedded tissues of pancreatic carcinomas].
Lei Gu, Quan-Cai Cui, J Chen, L Li, T Liu
Abstract
Lei Gu, Quan-Cai Cui, J Chen, L Li, T Liu
Abstract
OBJECTIVE: To examine the alteration and significance of the DPC4 gene in paraffin-embedded tissues of pancreatic carcinomas. METHODS: Polymerase chain reaction and single-strand conformation polymorphism analysis were used to search for deletions and mutations in the DPC4 gene in 46 cases of pancreatic carcinomas. RESULTS: Thirteen of forty-six (28.3%) cases were found to have homozygous deletions in exon 1, 2, 3, 4, 8 and 11. One was in exon 11, one in exon 1 and 11, one in exon 2 and 3, one in exon 3 and 8, one in exon 1, 2 and 8, one in exon 2, 4 and 11, one in exon 3, 4 and 11, three in exon 3, 4 and 8, one in exon 2, 3, 4, and 8, one in exon 2, 3, 8 and 11, one in exon 2, 3, 4, 8 and 11. Intragenic mutations were found in 10 of 46 cases (21.7%). One case was in exon 1, one in exon 2, three in exon 8, four in exon 11, and one in exon 4 and 11. The total frequency of intragenic changes of DPC4 in paraffin-embedded tissues was 45.6% (21/46). CONCLUSION: Inactivation of tumor-suppressor gene DPC4 may play an important role during the tumorigenesis of pancreatic carcinomas.
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OBJECTIVE: To examine the alteration and significance of the DPC4 gene in paraffin-embedded tissues of pancreatic carcinomas. METHODS: Polymerase chain reaction and single-strand conformation polymorphism analysis were used to search for deletions and mutations in the DPC4 gene in 46 cases of pancreatic carcinomas. RESULTS: Thirteen of forty-six (28.3%) cases were found to have homozygous deletions in exon 1, 2, 3, 4, 8 and 11. One was in exon 11, one in exon 1 and 11, one in exon 2 and 3, one in exon 3 and 8, one in exon 1, 2 and 8, one in exon 2, 4 and 11, one in exon 3, 4 and 11, three in exon 3, 4 and 8, one in exon 2, 3, 4, and 8, one in exon 2, 3, 8 and 11, one in exon 2, 3, 4, 8 and 11. Intragenic mutations were found in 10 of 46 cases (21.7%). One case was in exon 1, one in exon 2, three in exon 8, four in exon 11, and one in exon 4 and 11. The total frequency of intragenic changes of DPC4 in paraffin-embedded tissues was 45.6% (21/46). CONCLUSION: Inactivation of tumor-suppressor gene DPC4 may play an important role during the tumorigenesis of pancreatic carcinomas.
Key concepts: Exon, Biology, Tandem exon duplication, Molecular biology, Carcinogenesis, Gene, Exon trapping, Mutation