Specific chromosomal aberrations and amplification of the AIB1 nuclear receptor coactivator gene in pancreatic carcinomas

To screen pancreatic carcinomas for chromosomal aberrations we have applied molecular cytogenetic techniques, including fluorescent in situ hybridizat ion, comparative genomic hybridization, and spectral karyotyping to a serie s of nine established cell lines. Comparative genomic hybridization reveale d recurring chromosomal gains on chromosome arms 3q, 5p, 7p, 8q, 12p, and 2 0q. Chromosome losses were mapped to chromosome arms 8p, 9p, 17p, 18q, 19p, and chromosome 21. The comparison with comparative genomic hybridization d ata from primary pancreatic tumors indicates that a specific pattern of chr omosomal copy number changes is maintained in cell culture. Metaphase chrom osomes from six cell lines were analyzed by spectral karyotyping, a techniq ue that allows one to visualize all chromosomes simultaneously in different colors, Spectral karyotyping identified multiple chromosomal rearrangement s, the majority of which were unbalanced. No recurring reciprocal transloca tion was detected. Cytogenetic aberrations were confirmed using fluorescent in situ hybridization with probes for the MDR gene and the tumor suppresso r genes p16 and DCC, Copy number increases on chromosome 20q were validated with a probe specific for the nuclear receptor coactivator AIB1 that maps to chromosome 20q12, Amplification of this gene was identified in six of ni ne pancreatic cancer cell lines and correlated with increased expression.