ArticleMayo Clinic proceedings2009
Fluorescence in situ hybridization to visualize genetic abnormalities in interphase cells of acinar cell carcinoma, ductal adenocarcinoma, and islet cell carcinoma of the pancreas.
Article in Mayo Clinic proceedings, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 26 citations in OpenAlex.
- New treatment insights into pancreatic acinar cell carcinoma: case report and literature review.Frontiers in oncology · 2023Review
- Pancreatic acinar cell carcinoma: A comprehensive review.World journal of gastroenterology · 2022Review
- Targeting the NTRK Fusion Gene in Pancreatic Acinar Cell Carcinoma: A Case Report and Review of the Literature.Journal of the National Comprehensive Cancer Network : JNCCN · 2021Review
- Pancreatic acinar cell carcinoma is associated withCancer biology & therapy · 2019Review
- Surgical and molecular pathology of pancreatic neoplasms.Diagnostic pathology · 2016Review
- TP53 alterations in pancreatic acinar cell carcinoma: new insights into the molecular pathology of this rare cancer.Virchows Archiv : an international journal of pathology · 2016Article
- Whole exome sequencing reveals recurrent mutations in BRCA2 and FAT genes in acinar cell carcinomas of the pancreas.Scientific reports · 2015Article
- Acinar Cell Carcinoma of the Pancreas: Overview of Clinicopathologic Features and Insights into the Molecular Pathology.Frontiers in medicine · 2015Review
- Pathology and genetics of pancreatic neoplasms with acinar differentiation.Seminars in diagnostic pathology · 2014Article
- APC alterations are frequently involved in the pathogenesis of acinar cell carcinoma of the pancreas, mainly through gene loss and promoter hypermethylation.Virchows Archiv : an international journal of pathology · 2014Article
- Pancreatic cancer genomes: toward molecular subtyping and novel approaches to diagnosis and therapy.Molecular diagnosis & therapy · 2013Review
- Evaluation of phosphatidylinositol-3-kinase catalytic subunit (PIK3CA) and epidermal growth factor receptor (EGFR) gene mutations in pancreaticobiliary adenocarcinoma.Journal of gastrointestinal oncology · 2013Article
- Use of panitumumab in the treatment of acinar cell carcinoma of the pancreas: A case report.Oncology letters · 2013Article
- Hybridization-based detection of Helicobacter pylori at human body temperature using advanced locked nucleic acid (LNA) probes.PloS one · 2013Article
- The physiognomy of Mayo Clinic Proceedings, 2010.Mayo Clinic proceedings · 2010Article
- Pathology and molecular genetics of pancreatic neoplasms.Cancer journal (Sudbury, Mass.)Review
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12 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTo 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
methodsBetween 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.
resultsFISH 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.
conclusionFISH 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.
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