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HOME > J Pathol Transl Med > Volume 38(3); 2004 > Article
Original Article Genomic Imbalances in Ependymoma by Degenerate Oligonucleotide Primed PCR-Comparative Genomic Hybridization.
Sung Hye Park, Gi Jin Kim, Min Kyung Kim, Hanseong Kim, Yoen Lim Suh, Sun Hwa Park
Journal of Pathology and Translational Medicine 2004;38(3):133-137
DOI: https://doi.org/
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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.

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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