Molecular Genetics of Pancreatic Cancer

摘要: In cancer, genome stability is compromised. Ductal adenocarcinoma of the pancreas no exception. Considerable progress in identification and characterization somatic and/or germline genetic alterations has provided mechanistic foundations this genetically complex disease. Numerous alterations, including chromosomal copy-number gains, amplifications homozygous deletions, loss heterozygosity (LOH) with without copy number reduction, balanced unbalanced structural re-arrangements, are commonly observed ( 1 – 4 ). Gross changes often complemented by smaller, more subtle affecting open reading frames proto-oncogenes, tumor suppressors, caretaker genes 5 8 Continued evaluation these additional yet-unidentified should translate into rational diagnostic treatment strategies. This chapter describes spectrum frequency ductal adenocarcinomas pancreas, as organized underlying presence two, largely mutually exclusive, types instability: instability (CIN) microsatellite (MIN). distinction justified, each type exhibits unique histologic molecular characteristics 9