help button home button Am J Pathol ASIP MEMBERSHIP
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dannenberg, H.
Right arrow Articles by Komminoth, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dannenberg, H.
Right arrow Articles by Komminoth, P.
(American Journal of Pathology. 2001;158:1937-1942.)
© 2001 American Society for Investigative Pathology

Short Communication

Differential Loss of Chromosome 11q in Familial and Sporadic Parasympathetic Paragangliomas Detected by Comparative Genomic Hybridization

Hilde Dannenberg*, Ronald R. de Krijger*, Jianming Zhao{dagger}, Ernst J.M. Speel{dagger}, Parvin Saremaslani{dagger}, Winand N. M. Dinjens*, Wolter J. Mooi*{ddagger}, Jürgen Roth{dagger}, Philipp U. Heitz{dagger} and Paul Komminoth{dagger}§

From the Josephine Nefkens Institute,*
Erasmus University Medical Center, Rotterdam, the Netherlands; the Department of Pathology,{dagger}
University of Zürich, Zürich, Switzerland; the Department of Pathology,{ddagger}
Netherlands Cancer Institute, Amsterdam, the Netherlands; and the Institute of Pathology,§
Hospital Baden, Baden, Switzerland

Parasympathetic paragangliomas (PGLs) represent neuroendocrine tumors arising from chief cells in branchiomeric and intravagal paraganglia, which share several histological features with their sympathetic counterpart sympathoadrenal paragangliomas. In recent years, genetic analyses of the familial form of PGL have attracted considerable interest. However, the majority of paragangliomas occurs sporadically and it remains to be determined whether the pathogenesis of sporadic paraganglioma resembles that of the familial form. Furthermore, data on comparative genetic aberrations are scarce. To provide fundamental cytogenetic data on sporadic and hereditary PGLs, we performed comparative genomic hybridization using directly fluorochrome-conjugated DNA extracted from 12 frozen and 4 paraffin-embedded tumors. The comparative genomic hybridization data were extended by loss of heterozygosity analysis of chromosome 11q. DNA copy number changes were found in 10 (63%) of 16 tumors. The most frequent chromosomal imbalance involved loss of chromosome 11. Six of seven familial tumors and two of nine sporadic tumors showed loss of 11q (86% versus 22%, P = 0.012). Deletions of 11p and 5p were found in two of nine sporadic tumors. We conclude that overall DNA copy number changes are infrequent in PGLs compared to sympathetic paragangliomas and that loss of chromosome 11 may be an important event in their tumorigenesis, particularly in familial paragangliomas.




This article has been cited by other articles:


Home page
 Ann. N. Y. Acad. Sci.Home page
R. R DE KRIJGER, F. H VAN NEDERVEEN, E. KORPERSHOEK, W. W DE HERDER, S. M.P.F DE MUINCK KEIZER-SCHRAMA, and W. N.M DINJENS
Frequent genetic changes in childhood pheochromocytomas.
Ann. N.Y. Acad. Sci., August 1, 2006; 1073: 166 - 176.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2001 by the American Society for Investigative Pathology.