Clinical Cancer Research Bridging the Lab and the Clinic in Cancer Medicine Infection and Cancer: Biology, Therapeutics, and Prevention
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Mihaila, D.
Right arrow Articles by Rempel, S. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mihaila, D.
Right arrow Articles by Rempel, S. A.
Clinical Cancer Research Vol. 9, 4435-4442, October 1, 2003
© 2003 American Association for Cancer Research


Molecular Oncology, Markers, Clinical Correlates

Meningiomas

Analysis of Loss of Heterozygosity on Chromosome 10 in Tumor Progression and the Delineation of Four Regions of Chromosomal Deletion in Common with Other Cancers

Dana Mihaila, Jorge A. Gutiérrez, Mark L. Rosenblum, Irene F. Newsham, Oliver Bögler and Sandra A. Rempel1 on behalf of NABTT CNS Consortium2

Hermelin Brain Tumor Center [D. M., M. L. R., I. F. N., O. B., S. A. R.] and Department of Neuropathology [J. A. G.], Henry Ford Health Sciences Center, Detroit, Michigan 48202

Purpose: Loss of heterozygosity (LOH) of alleles on chromosome 10 has been reported in many cancers, leading to the identification of tumor suppressor genes on this chromosome. Several reports implicate LOH of chromosome 10 alleles in meningioma progression, but the frequency and complexity of the loss have not been well characterized. Furthermore, the location and identity of the putative tumor suppressor genes on this chromosome that contribute to meningioma progression are unknown because the currently characterized tumor suppressor genes do not appear to be involved. Therefore, this study was undertaken to (a) assess the frequency and complexity of LOH in meningioma progression, (b) map the LOH patterns of individual meningiomas to define the smallest regions of shared chromosomal deletion, and (c) compare the identified regions with chromosome 10 deletions in other cancers, and thereby initiate the localization of the putative tumor suppressor genes.

Experimental Design: We examined 11 microsatellite dinucleotide repeat loci in 208 meningiomas of all grades using laser capture microdissection and fluorescence-based detection of PCR products.

Results: For all markers examined, the incidence of LOH was much higher in all grades than that previously reported, with incidence and complexity of LOH increasing with tumor grade. LOH mapping identified four regions of chromosomal deletion: 10pter-D10S89, D10S109-D10S215, D10S187-D10S209, and D10S169-10qter. These deletions on chromosome 10 are shared with other cancer types.

Conclusions: These results delineate chromosomal locations of putative tumor suppressor genes on chromosome 10 that likely play an early role in meningioma tumorigenesis as well as tumor progression.




This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
C. H. Holschneider, R. L. Baldwin, K. Tumber, C. Aoyama, and B. Y. Karlan
The Fragile Histidine Triad Gene: A Molecular Link Between Cigarette Smoking and Cervical Cancer
Clin. Cancer Res., August 15, 2005; 11(16): 5756 - 5763.
[Abstract] [Full Text] [PDF]


Home page
Cancer Epidemiol. Biomarkers Prev.Home page
D. Cui, G. Jin, T. Gao, T. Sun, F. Tian, G. G. Estrada, H. Gao, and A. Sarai
Characterization of BRCAA1 and Its Novel Antigen Epitope Identification
Cancer Epidemiol. Biomarkers Prev., July 1, 2004; 13(7): 1136 - 1145.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2003 by the American Association for Cancer Research.