Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Ess, K. C.
Right arrow Articles by Gutmann, D. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ess, K. C.
Right arrow Articles by Gutmann, D. H.
NEUROLOGY 2005;64:1446-1449
© 2005 American Academy of Neurology


Brief Communications

Developmental origin of subependymal giant cell astrocytoma in tuberous sclerosis complex

Kevin C. Ess, MD, PhD, Christine A. Kamp, BS, Benjamin P. Tu, MD, PhD and David H. Gutmann, MD, PhD

From the Departments of Neurology (Drs. Ess and Gutmann, and C.A. Kamp) and Pathology (Dr. Tu), Division of Neuropathology, Washington University School of Medicine, St. Louis, MO.

Address correspondence and reprint requests to Dr. David H. Gutmann, Department of Neurology, Washington University School of Medicine, Box 8111, 660 South Euclid Avenue, St. Louis, MO 63110; e-mail: gutmannd{at}neuro.wustl.edu

Children with tuberous sclerosis complex (TSC) harbor developmental brain abnormalities (cortical tubers) and low-grade tumors (subependymal giant cell astrocytomas [SEGAs]). Using gene expression profiling to identify neuroglial differentiation markers in Tsc1 conditional knockout mice, the authors demonstrate that giant cells of SEGAs aberrantly express similar neuroglial differentiation markers as do cortical tubers. These results suggest that both tubers and SEGAs result from related defects in progenitor cell differentiation during brain development.


Supported by grants from the Department of Defense (DAMD17–03–1–0073; D.H.G.) and the National Institutes of Health (5T32-NS07205–21; K.C.E.).

Received September 16, 2004. Accepted in final form December 30, 2004.




This article has been cited by other articles:


Home page
J. Neurosci.Home page
L. Meikle, D. M. Talos, H. Onda, K. Pollizzi, A. Rotenberg, M. Sahin, F. E. Jensen, and D. J. Kwiatkowski
A Mouse Model of Tuberous Sclerosis: Neuronal Loss of Tsc1 Causes Dysplastic and Ectopic Neurons, Reduced Myelination, Seizure Activity, and Limited Survival
J. Neurosci., May 23, 2007; 27(21): 5546 - 5558.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by AAN Enterprises, Inc.