Pancreatic acinar carcinoma shows a distinct pattern of chromosomal imbalances by comparative genomic hybridization

Pancreatic acinar cell carcinoma (PAC) is a rare pancreatic tumor for which no information about chromosomal anomalies is available. We examined six p rimary PACs by comparative genomic hybridization (CGH). All cases showed ch romosomal changes. A total of 106 gains and 48 losses was detected. Consens us regions of gain were identified on chromosomes 1, 12, and X: 1q21 in fou r cases,1q42 in three cases, 12p11.2 in four cases, and Xq12-21 in three ca ses. Recurrent losses were found at 16p13.2-p13.1 in three cases and at 16q 23 in three cases. To verify these chromosomal imbalances, microsatellite a nalysis of matched normal and tumor DNA was performed using PCR-amplified m arkers for chromosomes 1, 12, and 16 in the regions showing nonrandom gains or losses. This analysis showed allelic imbalances in tumor DNA consistent with the CGH profiles. Our CGH study suggests that PAC shows a characteris tic pattern of chromosomal alterations, involving gain at 1 q, 12p, and Xq and loss of sequences at 16p and 16q. This pattern appears unique among sol id rumors and is markedly different from that detected in pancreatic ductal carcinomas by the same technique. This suggests that PAC tumorigenesis inv olves different molecular pathways than those involved in the more common p ancreatic ductal tumors. (C) 2000 Wiley-iiss, Inc.