PMID- 19720778 OWN - NLM STAT- MEDLINE DCOM- 20090921 LR - 20240322 IS - 1942-5546 (Electronic) IS - 0025-6196 (Print) IS - 0025-6196 (Linking) VI - 84 IP - 9 DP - 2009 Sep TI - Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas. PG - 801-10 LID - S0025-6196(11)60490-4 [pii] LID - 10.4065/84.9.801 [doi] AB - OBJECTIVE: To use fluorescence in situ hybridization (FISH) to visualize genetic abnormalities in interphase cell nuclei (interphase FISH) of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas. PATIENTS AND METHODS: Between April 4, 2007, and December 4, 2008, interphase FISH was used to study paraffin-embedded preparations of tissue obtained from 18 patients listed in the Mayo Clinic Biospecimen Resource for Pancreas Research with a confirmed diagnosis of acinar cell carcinoma, ductal adenocarcinoma, islet cell carcinoma, or pancreas without evidence of neoplasia. FISH probes were used for chromosome loci of APC (see glossary at end of article for expansion of all gene symbols), BRCA2, CTNNB1, EGFR, ERBB2, CDKN2A, TP53, TYMP, and TYMS. These FISH probes were used with control probes to distinguish among various kinds of chromosome abnormalities of number and structure. RESULTS: FISH abnormalities were observed in 12 (80%) of 15 patients with pancreatic cancer: 5 of 5 patients with acinar cell carcinoma, 5 of 5 patients with ductal adenocarcinoma, and 2 (40%) of 5 patients with islet cell carcinoma. All 3 specimens of pancreatic tissue without neoplasia had normal FISH results. Gains of CTNNB1 due to trisomy 3 occurred in each tumor with acinar cell carcinoma but in none of the other tumors in this study. FISH abnormalities of all other cancer genes studied were observed in all forms of pancreatic tumors in this investigation. CONCLUSION: FISH abnormalities of CTNNB1 due to trisomy 3 were observed only in acinar cell carcinoma. FISH abnormalities of genes implicated in familial cancer, tumor progression, and the 5-fluorouracil pathway were common but were not associated with specific types of pancreatic cancer. FAU - Dewald, Gordon W AU - Dewald GW AD - Division of Laboratory Genetics, Mayo Clinic, Rochester, MN 55905, USA. gdewald@mayo.edu FAU - Smyrk, Thomas C AU - Smyrk TC FAU - Thorland, Erik C AU - Thorland EC FAU - McWilliams, Robert R AU - McWilliams RR FAU - Van Dyke, Daniel L AU - Van Dyke DL FAU - Keefe, Jeannette G AU - Keefe JG FAU - Belongie, Kimberly J AU - Belongie KJ FAU - Smoley, Stephanie A AU - Smoley SA FAU - Knutson, Darlene L AU - Knutson DL FAU - Fink, Stephanie R AU - Fink SR FAU - Wiktor, Anne E AU - Wiktor AE FAU - Petersen, Gloria M AU - Petersen GM LA - eng GR - P50 CA102701/CA/NCI NIH HHS/United States GR - P20 CA102701/CA/NCI NIH HHS/United States GR - R01 CA97075/CA/NCI NIH HHS/United States GR - P50 CA102701-07/CA/NCI NIH HHS/United States GR - R01 CA097075/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PL - England TA - Mayo Clin Proc JT - Mayo Clinic proceedings JID - 0405543 SB - IM MH - Carcinoma, Acinar Cell/*genetics/pathology MH - Carcinoma, Islet Cell/*genetics/pathology MH - Carcinoma, Pancreatic Ductal/*genetics/pathology MH - *Chromosome Aberrations MH - Female MH - Humans MH - In Situ Hybridization, Fluorescence MH - Interphase/genetics MH - Male MH - Pancreatic Neoplasms/*genetics/pathology PMC - PMC2735430 EDAT- 2009/09/02 06:00 MHDA- 2009/09/22 06:00 PMCR- 2010/03/01 CRDT- 2009/09/02 09:00 PHST- 2009/09/02 09:00 [entrez] PHST- 2009/09/02 06:00 [pubmed] PHST- 2009/09/22 06:00 [medline] PHST- 2010/03/01 00:00 [pmc-release] AID - S0025-6196(11)60490-4 [pii] AID - 0840801 [pii] AID - 10.4065/84.9.801 [doi] PST - ppublish SO - Mayo Clin Proc. 2009 Sep;84(9):801-10. doi: 10.4065/84.9.801.