Document Detail


Genetic evidence for early divergence of small functioning and nonfunctioning endocrine pancreatic tumors: gain of 9Q34 is an early event in insulinomas.
MedLine Citation:
PMID:  11431358     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The malignant potential among endocrine pancreatic tumors (EPTs) varies greatly and can frequently not be predicted using histopathological parameters. Thus, molecular markers that can predict the biological behavior of EPTs are required. In a previous comparative genomic hybridization study, we observed marked genetic differences between the various EPT subtypes and a correlation between losses of 3p and 6 and gains of 14q and Xq and metastatic disease. To search for genetic alterations that play a role during early tumor development, we have studied 38 small (< or =2 cm) EPTs, including 24 insulinomas and 10 nonfunctioning EPTs. Small EPTs are usually classified as clinically benign tumors in the absence of histological signs of malignancy. Using comparative genomic hybridization, we identified chromosomal aberrations in 27 EPTs (mean, 4.1). Interestingly, the number of gains differed strongly between nonfunctioning and functioning EPTs (3.4 versus 1.5, respectively; P = 0.0526), as did the number of aberrations in the benign (n = 30) and malignant (n = 8) tumors (3 versus 8.4, respectively; P = 0.0022). In the insulinomas, 9q gain (common region of involvement: 9q34) was most common (50%) and in nonfunctioning EPTs, gain of 4p was most common (40%). Most frequent losses in insulinomas involved 1p (20.8%), 1q, 4q, 11q, Xq, and Y (all 16.7%) and in nonfunctioning EPTs, 6q. Losses of 3pq and 6q and gains of 17pq and 20q proved to be strongly associated with malignant behavior in all of the small EPTs (P < or = 0.0219). Our results demonstrate marked genetic differences between small functioning and nonfunctioning EPTs, indicating that these subtypes evolve along different genetic pathways. In addition, our study endorses the importance of chromosomes 3 and 6q losses to discriminate EPTs with a malignant behavior from benign ones.
Authors:
E J Speel; A F Scheidweiler; J Zhao; C Matter; P Saremaslani; J Roth; P U Heitz; P Komminoth
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cancer research     Volume:  61     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2001 Jul 
Date Detail:
Created Date:  2001-06-29     Completed Date:  2001-07-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5186-92     Citation Subset:  IM    
Affiliation:
Department of Molecular Cell Biology, University of Maastricht, Research Institute Growth and Development, 6200 MD Maastricht, The Netherlands. ernstjan.speel@molcelb.unimaas.nl
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Aged
Aged, 80 and over
Chromosome Aberrations*
Chromosome Deletion
Chromosomes, Human, Pair 3
Chromosomes, Human, Pair 6
Chromosomes, Human, Pair 9*
Female
Humans
In Situ Hybridization, Fluorescence
Insulinoma / genetics*,  pathology
Male
Middle Aged
Nucleic Acid Hybridization
Pancreatic Neoplasms / classification,  genetics*,  pathology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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