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

Domenica Taruscio, Silvia Paradisi, Giuseppe Zamboni, Gildas Rigaud, Massimo Falconi, Aldo Scarpa

Research output: Contribution to journalArticlepeer-review


Pancreatic acinar cell carcinoma (PAC) is a rare pancreatic tumor for which no information about chromosomal anomalies is available. We examined six primary PACs by comparative genomic hybridization (CGH). All cases showed chromosomal changes. A total of 106 gains and 48 losses was detected. Consensus regions of gain were identified on chromosomes 1, 12, and X: 1q21 in four cases, 1q42 in three cases, 12p11.2 in four cases, and Xq12-21 in three cases. Recurrent losses were found at 16p13.2-p13.1 in three cases and at 16q23 in three cases. To verify these chromosomal imbalances, microsatellite analysis of matched normal and tumor DNA was performed using PCR-amplified markers 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 characteristic pattern of chromosomal alterations, involving gain at 1q, 12p, and Xq and loss of sequences at 16p and 16q. This pattern appears unique among solid tumors and is markedly different from that detected in pancreatic ductal carcinomas by the same technique. This suggests that PAC tumorigenesis involves different molecular pathways than those involved in the more common pancreatic ductal tumors. (C) 2000 Wiley-Liss, Inc.

Original languageEnglish
Pages (from-to)294-299
Number of pages6
JournalGenes Chromosomes and Cancer
Issue number3
Publication statusPublished - Jul 2000

ASJC Scopus subject areas

  • Cancer Research
  • Genetics


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