Non-random chromosomal rearrangements in pancreatic cancer cell lines identified by spectral karyotyping

The molecular events involved in pancreatic cancer are becoming increasingl y well characterized, with mutations in the dominant oncogene KRAS and the tumour suppressor genes TP53, CDKN2A and MADH4 being typically observed. Ho wever, other genetic abnormalities remain to be identified and molecular cy togenetics may be useful to detect chromosomal loci involved in recurrent r earrangements. We have used spectral karyotyping to characterize cytogeneti c aberrations in a panel of 20 human pancreatic carcinoma cell lines and co nfirmed their identities by dual and triple color fluorescence in situ hybr idization. The most common partial or whole-arm gains involved 5p, 7q, 12p, 1q, 7p, 5q, 9p, 9q and 11p. The most common partial or whole-arm losses af fected 9p, 11q, 18q, 3p, 2q and 1p, as well as the short arms of the acroce ntric chromosomes. Spectral karyotyping allowed us to identify a number of recurrent structural aberrations, all of them unbalanced: most frequently i (5)(p10), del(11)(q23), i(12)(p10), i(1)(q10), del(7)(q22) and del(10)(p11) . Spectral karyotyping mapped the complex aberrations occurring in pancreat ic cancer cell lines and identified non-random patterns of chromosomal rear rangement. This comprehensive characterization should be useful to direct f uture investigation. The observation that loss at i Iq and gains at 5p with i(5)(p10) and 12p with i(12)(p10) are more frequent changes than previousl y reported would justify more intensive investigation of these chromosomal regions. (C) 2001 Wiley-Liss, Inc.