| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6145
To better understand the molecular mechanisms responsible for meningioma tumorigenesis we previously utilized subtractive hybridization protocols to identify genes the expression or structure of which is altered in these common brain tumors. Here we show that a CA dinucleotide repeat element present in one complementary DNA isolated by this approach has undergone a contraction in size in a meningioma cell line. Extension of this initial observation has revealed widespread genetic alterations affecting simple repeat sequences in this and other meningiomas. These data indicate that genetic instability may play a previously unrecognized role in the etiology of meningiomas.
1 This work was supported by NIH-USPHS Grant NS30025; M. P. was supported in part by NIH-USPHS Training Grant 5-T32-GM07170.
2 Present address: Department of Molecular Biology, Princeton University, Princeton, NJ 08544.
3 To whom requests for reprints should be addressed, at Room 445 Clinical Research Building, 415 Curie Boulevard, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6145.
Received 8/25/94. Accepted 11/ 1/94.
This article has been cited by other articles:
![]() |
M. J. Sobrido, C. R. Pereira, F. Barros, J. Forteza, A. Carracedo, and M. Lema Low frequency of replication errors in primary nervous system tumours J. Neurol. Neurosurg. Psychiatry, September 1, 2000; 69(3): 369 - 375. [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 |