Pancreatic cancer is a devastating disease with an extremely poor prognosis, and thus, there is a great need for better diagnostic and therapeutic tools. The 19q13 chromosomal locus is amplified in several cancer types, including pancreatic cancer, but the possible clinical significance of this aberration remains unclear. We used fluorescence in situ hybridization on tissue microarrays containing 357 primary pancreatic tumors, 151 metastases, and 24 local recurrences as well as 120 cancer cell lines from various tissues to establish the frequency of the 19q13 amplification and to find potential correlations to clinical parameters including patient survival. Copy number increases were found in 12.2% of the primary pancreatic tumors and 9.3% of the cell lines, including those derived from bladder, colorectal, ovarian, and thyroid carcinomas. Copy number changes were linked to high grade (P = 0.044) and stage (P = 0.025) tumors, and the average survival time of patients with 19q13 amplification was shorter than that of those without this aberration. Our findings revealed recurrent 19q13 amplification in pancreatic cancer and involvement of the same locus as in bladder, colorectal, ovarian, and thyroid carcinomas. More importantly, the 19q13 amplifications were associated with poor tumor phenotype and showed a trend toward shorter survival.
Pancreatic cancer is a devastating disease with an extremely poor prognosis, and thus, there is a great need for better diagnostic and therapeutic tools. The 19q13 chromosomal locus is amplified in several cancer types, including pancreatic cancer, but the possible clinical significance of this aberration remains unclear. We used fluorescence in situ hybridization on tissue microarrays containing 357 primary pancreatic tumors, 151 metastases, and 24 local recurrences as well as 120 cancer cell lines from various tissues to establish the frequency of the 19q13 amplification and to find potential correlations to clinical parameters including patient survival. Copy number increases were found in 12.2% of the primary pancreatic tumors and 9.3% of the cell lines, including those derived from bladder, colorectal, ovarian, and thyroid carcinomas. Copy number changes were linked to high grade (P = 0.044) and stage (P = 0.025) tumors, and the average survival time of patients with 19q13 amplification was shorter than that of those without this aberration. Our findings revealed recurrent 19q13 amplification in pancreatic cancer and involvement of the same locus as in bladder, colorectal, ovarian, and thyroid carcinomas. More importantly, the 19q13 amplifications were associated with poor tumor phenotype and showed a trend toward shorter survival.