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Genomic Imbalances in Ependymoma by Degenerate Oligonucleotide Primed PCR-Comparative Genomic Hybridization

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¹Ú¼ºÇý, ±èÇѼº, ¹Ú¼±È­, ±è¹Î°æ, ±è±âÁø, Suh Yoen-Lim,
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¹Ú¼ºÇý ( Park Sung-Hye ) 
¼­¿ï´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç

±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 ) 
¼º±Õ°ü´ëÇб³ ÀÇ°ú´ëÇÐ »ï¼º¼­¿ïº´¿ø º´¸®°ú

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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KCI
KoreaMed
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