作者: K. Brune , S.-M. Hong , A. Li , S. Yachida , T. Abe
DOI: 10.1158/1055-9965.EPI-08-0630
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摘要: Background: Little is known about the genetic and epigenetic changes that contribute to familial pancreatic cancers. The aim of this study was compare prevalence common alterations in sporadic ductal adenocarcinomas. Methods: DNA isolated from microdissected cancers 39 patients with 36 adenocarcinoma. KRAS2 mutations were detected by Bst N1 digestion and/or cycle sequencing. TP53 SMAD4 status determined immunohistochemistry on tissue microarrays 23 archival adenocarcinomas selected cases sequencing identify gene mutations. Methylation-specific PCR analysis seven genes ( FoxE1, NPTX2, CLDN5, P16, TFPI-2, SPARC, ppENK ) done a subset fresh-frozen adenocarcinomas. Results: identified 31 (80%) versus 28 (78%) Positive immunolabeling for p53 observed 57% loss labeling 61% cancers, rates similar those mean aberrant methylation 68.4%, which not significantly different cancers. Conclusion: mutant , inactivation seven-gene panel as adenocarcinomas. These findings support use markers detect (Cancer Epidemiol Biomarkers Prev 2008;17(12):3536–42)