Chromosomal abnormalities of adenocarcinoma of the pancreas: identifying early and late changes

摘要: Abstract The high level of karyotypic complexity found in epithelial neoplasms hinders the characterization their cytogenetic evolution. Derivation such pathways adenocarcinoma pancreas has been particularly limited, because only a few pancreatic carcinomas are resected at an early stage disease and so number primary for which analysis abnormal karyotypes reported is small. Here we report clonal abnormalities identified by G-banding 36 obtained from patients undergoing Whipple resection with curative intent. majority were diploid or triploid (33 36; 91%). Numerical alterations all complete karyotype was determined. All chromosomes involved gain, loss, both gain loss entire chromosome, least 8 up to 28 carcinomas. Most commonly lost 18 (in 78% carcinomas), 17 (56%), 6 (44%), 21 (42%), 22 Y (36%), 4 (33%). Gain chromosome 20 observed 10 Structural common, resulting partial chromosomal gains losses, median 7 imbalances per carcinoma (range, 1–15). Sixteen contained double-minute chromosomes, homogeneously staining regions, both, indicating gene amplification. Pooling data these published Mitelman database ( http://cgap.nci.nih.gov/Chromosomes/Mitelman ), defined most frequent −18 (67.6%), −10 (34.3%), −4 (31.4%), +20 −15p (23.8%), −14p (22.9%), +2 (21.9%), −5 −13p (20%), +16 −21p (19%), −17p +1q (19.0%). Recurrent as occurring −1p, −15p, −18, −7q, −8p, −17p, −5; late recurrent +11q, +7q, +6p, −19p, +2. In contrast reports similar analyses other carcinomas, did not find evidence multiple evolutionary pathways.