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Article: Identification of novel regions of allelic loss in ependymomas by high-resolution allelotyping with 384 microsatellite markers

TitleIdentification of novel regions of allelic loss in ependymomas by high-resolution allelotyping with 384 microsatellite markers
Authors
KeywordsComparative genomic hybridization
Ependymoma
Loss of heterozygosity
Overlapping small deletion region
Issue Date2001
Citation
Journal of Neurosurgery, 2001, v. 95, n. 1, p. 9-14 How to Cite?
AbstractObject. Ependymomas are rare glial neoplasms; little is known about the molecular pathogenesis of this tumor entity. In a previous study the authors found multiple genomic imbalances in ependymomas resected in 20 adults and eight children, including loss of chromosomes 1p, 6, 16, 17, 19q, 20q, and 22q, as well as gain of chromosomes 4q, 5q, 7q, 9q, and 12q on comparative genomic hybridization. The aim of this study was to map in more detail the commonly affected regions in ependymomas. Methods. A comprehensive allelotype analysis of 16 ependymomas was conducted using 384 microsatellite markers that span the 22 autosomes. Based on this high-resolution loss of heterozygosity analysis, multiple over- lapping deletion regions were identified as follows: 6q25.2-27, 16p12-13.1, 16q22.3-24.1, 17q22-24, 19q12-13.2, 20q13.2-13.3, and 22q13.1-13.3. Conclusions. These data confirmed previous reports that loss of chromosomes 17 and 22 were common in ependymomas. Moreover, the authors were able to identify loss of chromosomes 13, 16, 19, and 20 as novel findings in ependymomas. It is believed that potential tumor suppressor genes that reside in these commonly deleted regions may contribute to the molecular tumorigenesis of ependymomas.
Persistent Identifierhttp://hdl.handle.net/10722/325033
ISSN
2023 Impact Factor: 3.5
2023 SCImago Journal Rankings: 1.173
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTong, C. Y.K.-
dc.contributor.authorPhil, M.-
dc.contributor.authorZheng, P. P.-
dc.contributor.authorPang, J. C.S.-
dc.contributor.authorPoon, W. S.-
dc.contributor.authorChang, A. R.-
dc.contributor.authorNg, H. K.-
dc.date.accessioned2023-02-27T07:29:09Z-
dc.date.available2023-02-27T07:29:09Z-
dc.date.issued2001-
dc.identifier.citationJournal of Neurosurgery, 2001, v. 95, n. 1, p. 9-14-
dc.identifier.issn0022-3085-
dc.identifier.urihttp://hdl.handle.net/10722/325033-
dc.description.abstractObject. Ependymomas are rare glial neoplasms; little is known about the molecular pathogenesis of this tumor entity. In a previous study the authors found multiple genomic imbalances in ependymomas resected in 20 adults and eight children, including loss of chromosomes 1p, 6, 16, 17, 19q, 20q, and 22q, as well as gain of chromosomes 4q, 5q, 7q, 9q, and 12q on comparative genomic hybridization. The aim of this study was to map in more detail the commonly affected regions in ependymomas. Methods. A comprehensive allelotype analysis of 16 ependymomas was conducted using 384 microsatellite markers that span the 22 autosomes. Based on this high-resolution loss of heterozygosity analysis, multiple over- lapping deletion regions were identified as follows: 6q25.2-27, 16p12-13.1, 16q22.3-24.1, 17q22-24, 19q12-13.2, 20q13.2-13.3, and 22q13.1-13.3. Conclusions. These data confirmed previous reports that loss of chromosomes 17 and 22 were common in ependymomas. Moreover, the authors were able to identify loss of chromosomes 13, 16, 19, and 20 as novel findings in ependymomas. It is believed that potential tumor suppressor genes that reside in these commonly deleted regions may contribute to the molecular tumorigenesis of ependymomas.-
dc.languageeng-
dc.relation.ispartofJournal of Neurosurgery-
dc.subjectComparative genomic hybridization-
dc.subjectEpendymoma-
dc.subjectLoss of heterozygosity-
dc.subjectOverlapping small deletion region-
dc.titleIdentification of novel regions of allelic loss in ependymomas by high-resolution allelotyping with 384 microsatellite markers-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.3171/jns.2001.95.1.0009-
dc.identifier.pmid11453403-
dc.identifier.scopuseid_2-s2.0-0034871190-
dc.identifier.volume95-
dc.identifier.issue1-
dc.identifier.spage9-
dc.identifier.epage14-
dc.identifier.isiWOS:000169622900002-

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