c-MYC amplification and c-myc protein expression in pancreatic acinar cell carcinomas. New insights into the molecular signature of these rare cancers.
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State: Public
Version: Author's accepted manuscript
State: Public
Version: Author's accepted manuscript
Serval ID
serval:BIB_1790DC6C319F
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
c-MYC amplification and c-myc protein expression in pancreatic acinar cell carcinomas. New insights into the molecular signature of these rare cancers.
Journal
Virchows Archiv
ISSN
1432-2307 (Electronic)
ISSN-L
0945-6317
Publication state
Published
Issued date
10/2018
Peer-reviewed
Oui
Volume
473
Number
4
Pages
435-441
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Publication Status: ppublish
Abstract
The molecular alterations of pancreatic acinar cell carcinomas (ACCs) and mixed acinar-neuroendocrine carcinomas (MANECs) are not completely understood, and the possible role of c-MYC amplification in tumor development, progression, and prognosis is not known. We have investigated c-MYC gene amplification in a series of 35 ACCs and 4 MANECs to evaluate its frequency and a possible prognostic role. Gene amplification was investigated using interphasic fluorescence in situ hybridization analysis simultaneously hybridizing c-MYC and the centromere of chromosome 8 probes. Protein expression was immunohistochemically investigated using a specific monoclonal anti-c-myc antibody. Twenty cases had clones with different polysomies of chromosome 8 in absence of c-MYC amplification, and 5 cases had one amplified clone and other clones with chromosome 8 polysomy, while the remaining 14 cases were diploid for chromosome 8 and lacked c-MYC amplification. All MANECs showed c-MYC amplification and/or polysomy which were observed in 54% pure ACCs. Six cases (15.3%) showed nuclear immunoreactivity for c-myc, but only 4/39 cases showed simultaneous c-MYC amplification/polysomy and nuclear protein expression. c-myc immunoreactivity as well as c-MYC amplification and/or chromosome 8 polysomy was not statistically associated with prognosis. Our study demonstrates that a subset of ACCs shows c-MYC alterations including gene amplification and chromosome 8 polysomy. Although they are not associated with a different prognostic signature, the fact that these alterations are present in all MANECs suggests a role in the acinar-neuroendocrine differentiation possibly involved in the pathogenesis of MANECs.
Keywords
Adult, Aged, Aged, 80 and over, Aneuploidy, Biomarkers, Tumor/analysis, Biomarkers, Tumor/genetics, Carcinoma, Acinar Cell/chemistry, Carcinoma, Acinar Cell/genetics, Carcinoma, Acinar Cell/pathology, Carcinoma, Acinar Cell/therapy, Cell Differentiation, Chromosomes, Human, Pair 8, Female, Gene Amplification, Genetic Predisposition to Disease, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Male, Middle Aged, Neoplasms, Complex and Mixed/chemistry, Neoplasms, Complex and Mixed/genetics, Neoplasms, Complex and Mixed/pathology, Neoplasms, Complex and Mixed/therapy, Neuroendocrine Tumors/chemistry, Neuroendocrine Tumors/genetics, Neuroendocrine Tumors/pathology, Neuroendocrine Tumors/therapy, Pancreatic Neoplasms/chemistry, Pancreatic Neoplasms/genetics, Pancreatic Neoplasms/pathology, Pancreatic Neoplasms/therapy, Phenotype, Prognosis, Proto-Oncogene Proteins c-myc/analysis, Proto-Oncogene Proteins c-myc/genetics, Transcriptome, Acinar cell carcinoma, Amplification, MANEC, MiNEN, Pancreas, c-myc
Pubmed
Web of science
Create date
08/05/2018 15:13
Last modification date
21/11/2022 9:29