| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Regular Articles |



From the Departments of Neurological Surgery*
and
Lab Medicine,¶
the Division of
Neuropathology,
the Brain Tumor Research
Center and Cancer Genetics Program,||
University of
California, San Francisco, California; the Department of Pathology and
Laboratory Medicine,
Mayo Clinic and
Foundation, Rochester, Minnesota; and the Department of Pathology and
Laboratory Medicine,§
Emory University,
Atlanta, Georgia
Ependymoma occurs most frequently within the central nervous system of children and young adults. We determined relative chromosomal copy-number aberrations in 44 ependymomas using comparative genomic hybridization. The study included 24 intracranial and 20 spinal cord tumors from pediatric and adult patients. Frequent chromosomal aberrations in intracranial tumors were gain of 1q and losses on 6q, 9, and 13. Gain of 1q and loss on 9 were preferentially associated with histological grade 3 tumors. On the other hand, gain on chromosome 7 was recognized almost exclusively in spinal cord tumors, and was associated with various other chromosomal aberrations including frequent loss of 22q. We conclude that cytogenetic analysis of ependymomas may help to classify these tumors and provide leads concerning their initiation and progression. The relationship of these aberrations to patient outcome needs to be addressed.
This article has been cited by other articles:
![]() |
P. Modena, E. Lualdi, F. Facchinetti, J. Veltman, J. F. Reid, S. Minardi, I. Janssen, F. Giangaspero, M. Forni, G. Finocchiaro, et al. Identification of Tumor-Specific Molecular Signatures in Intracranial Ependymoma and Association With Clinical Characteristics J. Clin. Oncol., November 20, 2006; 24(33): 5223 - 5233. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. Mendrzyk, A. Korshunov, A. Benner, G. Toedt, S. Pfister, B. Radlwimmer, and P. Lichter Identification of gains on 1q and epidermal growth factor receptor overexpression as independent prognostic markers in intracranial ependymoma. Clin. Cancer Res., April 1, 2006; 12(7): 2070 - 2079. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Korshunov, K. Neben, G. Wrobel, B. Tews, A. Benner, M. Hahn, A. Golanov, and P. Lichter Gene Expression Patterns in Ependymomas Correlate with Tumor Location, Grade, and Patient Age Am. J. Pathol., November 1, 2003; 163(5): 1721 - 1727. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Dyer, E. Prebble, V. Davison, P. Davies, P. Ramani, D. Ellison, and R. Grundy Genomic Imbalances in Pediatric Intracranial Ependymomas Define Clinically Relevant Groups Am. J. Pathol., December 1, 2002; 161(6): 2133 - 2141. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Gilbertson, L. Bentley, R. Hernan, T. T. Junttila, A. J. Frank, H. Haapasalo, M. Connelly, C. Wetmore, T. Curran, K. Elenius, et al. ERBB Receptor Signaling Promotes Ependymoma Cell Proliferation and Represents a Potential Novel Therapeutic Target for This Disease Clin. Cancer Res., October 1, 2002; 8(10): 3054 - 3064. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Sonoda, T. Ozawa, Y. Hirose, K. D. Aldape, M. McMahon, M. S. Berger, and R. O. Pieper Formation of Intracranial Tumors by Genetically Modified Human Astrocytes Defines Four Pathways Critical in the Development of Human Anaplastic Astrocytoma Cancer Res., July 1, 2001; 61(13): 4956 - 4960. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |