Comparison of Chromosomal Abnormalities by Fluorescence In Situ Hybridization between Intraductal Papillary Mucinous Neoplasm and Pancreatic Ductal Adenocarcinoma
Katsuyuki Miyabe, Hiroshi Inagaki, Takahiro Nakazawa, Kaduki Hayashi, Itaru Naitoh, Shuya Shimizu, Hiromu Kondo, Mitihiro Yoshida, Hiroaki Yamashita, Shuichiro Umemura, Yasuki Hori, Hirotaka Ohara, Takashi Joh. Nagoya City University, Nagoya, Japan
Background: Diagnosis of pancreatic malignancy on cytological specimen by fluorescence in situ hybridization (FISH) has been recently reported; however, few comparative studies of chromosomal abnormalities between intraductal papillary mucinous neoplasm (IPMN) and pancreatic ductal adenocarcinoma (PDAC) using FISH have been reported so far. The aim of this study is to examine the difference of chromosomal and locus abnormalities between IPMN and PDAC.
Design: Resected specimens of IPMN with low or intermediate-grade dysplasia (IPMN; n=15; gastric type: intestinal type = 12:3), PDAC (n=22; differentiation, well: moderate: poor = 9:11:2), and normal pancreatic ductal epithelial cells as controls (NM; n=18) were gathered. FISH analysis was performed to detect aneuploidies of chromosome (3, 6, 7, 8, 17, and 18) and loss of gene (p16 at 9p21 and p53 at 17p13). We evaluated chromosome (monosomy and polysomy) and locus (hemizygous deletion and homozygous deletion) abnormalities in IPMN and PDAC by comparison with NM. Furthermore, we compared these differences between IPMN and PDAC.
Results: Polysomies of chromosome 6, 7, 17, and 18 were significantly more frequent in PDAC than IPMN (chromosome 6, 12/22 vs 2/15, p=0.016; chromosome 7, 16/22 vs 3/15, p=0.003; chromosome 17, 13/22 vs 1/15, p=0.002; chromosome 18, 9/22 vs 1/15, p=0.028, respectively). Any kinds of monosomies did not differ significantly between IPMN and PDAC. The number of polysomy was significantly more in PDAC than IPMN (2.9±1.6 vs 0.8±1.1; P<0.0001). If specimen with polysomy 6 or 17 was considered positive for PDAC, the sensitivity and specificity were 100% and 80%, respectively. Loss of p16 and p53 was significantly more common in PDAC than in IPMN (p16, 12/22 vs 2/15, p=0.0164; p53, 13/22 vs 0/15, p=0.0002, respectively). Most of these deletions in PDAC were homozygous (p16, 11/12, 82%; p53, 12/13, 92%).
Conclusions: Our study reveals that chromosome and locus abnormalities correlate to pancreatic tumor malignancies and FISH is a useful modality to differentiate PDAC from IPMN.
Tuesday, March 5, 2013 1:00 PM
Poster Session IV # 163, Tuesday Afternoon