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Genomic Imbalances in Ependymoma by Degenerate Oligonucleotide Primed PCR-Comparative Genomic Hybridization변성올리고핵산염으로 감작된 중합효소연쇄반응과 게놈비교보합법으로 연구한 뇌실막세포종의 유전체불균형
- Other Titles
- 변성올리고핵산염으로 감작된 중합효소연쇄반응과 게놈비교보합법으로 연구한 뇌실막세포종의 유전체불균형
- Issue Date
- Jun-2004
- Publisher
- 대한병리학회
- Keywords
- Ependymoma; Comparative Genomic Hybridization; Chromosomal aberration; PCR
- Citation
- Journal of Pathology and Translational Medicine, v.38, no.3, pp 133 - 137
- Pages
- 5
- Journal Title
- Journal of Pathology and Translational Medicine
- Volume
- 38
- Number
- 3
- Start Page
- 133
- End Page
- 137
- ISSN
- 2383-7837
2383-7845
- 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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Related Researcher
- Park, Sun Hwa
- College of Medicine (Department of Anatomy)