Genomic Imbalances in Ependymoma by Degenerate Oligonucleotide Primed PCR-Comparative Genomic Hybridization
¹Ú¼ºÇý, ±èÇѼº, ¹Ú¼±È, ±è¹Î°æ, ±è±âÁø, Suh Yoen-Lim,
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¹Ú¼ºÇý ( Park Sung-Hye )
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±èÇѼº ( Kim Han-Seong )
ÀÎÁ¦´ëÇб³ ÀÇ°ú´ëÇÐ ÀÏ»ê¹éº´¿ø º´¸®°ú
¹Ú¼±È ( Park Sun-Hwa )
°í·Á´ëÇб³ ÀÇ°ú´ëÇÐ ÇغÎÇб³½Ç
±è¹Î°æ ( Kim Min-Kyung )
ÀÎÁ¦´ëÇб³ ÀÇ°ú´ëÇÐ ÀÏ»ê¹éº´¿ø º´¸®°ú
±è±âÁø ( Kim Gi-Jin )
°í·Á´ëÇб³ ÀÇ°ú´ëÇÐ ÇغÎÇб³½Ç
( Suh Yoen-Lim )
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KMID : 0357920040380030133
Abstract
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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Ependymoma;Comparative Genomic Hydridization;Chromosomal aberration;PCR
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