Korean J Pathol.
2004 Jun;38(3):133-137.
Genomic Imbalances in Ependymoma by Degenerate Oligonucleotide Primed PCR-Comparative Genomic Hybridization
- Affiliations
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- 1Department of Pathology, Seoul National University, College of Medicine, Seoul, Korea. parksh@korea.ac.kr
- 2Institute of Human Genetics, Department of Anatomy, Brain Korea 21 Biomedical Sciences, Korea University College of Medicine, Seoul, Korea.
- 3Department of Pathology, Ilsanpaik Hospital, Inje University, College of Medicine, Goyang, Korea.
- 4Department of Pathology, Samsung Medical Center, Sungkyungkwan University School of Medicine, Seoul, Korea.
Abstract
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BACKGROUND: The most consistent chromosomal abnormality in ependymomas, is loss of 22q (17-75%) and gain of 1q (0-50%). However, significance of this abnormality is uncertain.
METHODS
Genomic imbalances in 27 Korean ependymomas, including 21 low grade ependymomas, 4 anaplastic and 2 myxopapillary ependymomas, were analyzed by degenerate oligonucleotide primed-PCR-comparative genomic hybridization.
RESULTS
Common gains were found in 17 (63%), 20q (59%), 9q34 (41%), 15q24-qter (33%), 11q13 (30%), 12q23 (26%), 7q23-qter (26%), 16q23-qter (30%), 19 (26%), and 1q32-qter (22%). DNA amplification was identified in 12 tumors (44%). Chromosomal loss was a less common occurrence in our study, but was found in 13q (26%), 6q (19%), and 3 (11%).
CONCLUSION
The recurrent gains or losses of the chromosomal regions which were identified in this study provide candidate regions that may be involved in the development and progression of ependymomas.
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