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Genetic abnormalities detected in ependymomas by comparative genomic hybridisation
Using comparative genomic hybridisation, we have analysed genetic imbalance in a series of 86 ependymomas from children and adults. Tumours were derived from intracranial and spinal sites, and classified histologically as classic, anaplastic or myxopapillary. Ependymomas showing a balanced profile w...
Autores principales: | , , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
2002
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364143/ https://www.ncbi.nlm.nih.gov/pubmed/11953826 http://dx.doi.org/10.1038/sj.bjc.6600180 |
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author | Carter, M Nicholson, J Ross, F Crolla, J Allibone, R Balaji, V Perry, R Walker, D Gilbertson, R Ellison, D |
author_facet | Carter, M Nicholson, J Ross, F Crolla, J Allibone, R Balaji, V Perry, R Walker, D Gilbertson, R Ellison, D |
author_sort | Carter, M |
collection | PubMed |
description | Using comparative genomic hybridisation, we have analysed genetic imbalance in a series of 86 ependymomas from children and adults. Tumours were derived from intracranial and spinal sites, and classified histologically as classic, anaplastic or myxopapillary. Ependymomas showing a balanced profile were significantly (P<0.0005) more frequent in children than adults. Profiles suggesting intermediate ploidy were common (44% of all tumours), and found more often (P<0.0005) in tumours from adults and the spinal region. Loss of 22q was the most common specific abnormality, occurring in 50% of spinal (medullary) ependymomas and 26% of tumours overall. Genetic profiles combining loss of 22q with other specific abnormalities – gain of 1q, loss of 6q, loss of 10q/10, loss of 13, loss of 14q/14 – varied according to site and histology. In particular, we showed that classic ependymomas from within the cranium and spine have distinct genetic profiles. Classic and anaplastic ependymomas with gain of 1q tended to occur in the posterior fossa of children and to behave aggressively. Our extensive data on ependymomas demonstrate significant associations between genetic aberrations and clinicopathological variables, and represent a starting point for further biological and clinical studies. British Journal of Cancer (2002) 86, 929–939. DOI: 10.1038/sj/bjc/6600180 www.bjcancer.com © 2002 Cancer Research UK |
format | Text |
id | pubmed-2364143 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23641432009-09-10 Genetic abnormalities detected in ependymomas by comparative genomic hybridisation Carter, M Nicholson, J Ross, F Crolla, J Allibone, R Balaji, V Perry, R Walker, D Gilbertson, R Ellison, D Br J Cancer Genetics and Genomics Using comparative genomic hybridisation, we have analysed genetic imbalance in a series of 86 ependymomas from children and adults. Tumours were derived from intracranial and spinal sites, and classified histologically as classic, anaplastic or myxopapillary. Ependymomas showing a balanced profile were significantly (P<0.0005) more frequent in children than adults. Profiles suggesting intermediate ploidy were common (44% of all tumours), and found more often (P<0.0005) in tumours from adults and the spinal region. Loss of 22q was the most common specific abnormality, occurring in 50% of spinal (medullary) ependymomas and 26% of tumours overall. Genetic profiles combining loss of 22q with other specific abnormalities – gain of 1q, loss of 6q, loss of 10q/10, loss of 13, loss of 14q/14 – varied according to site and histology. In particular, we showed that classic ependymomas from within the cranium and spine have distinct genetic profiles. Classic and anaplastic ependymomas with gain of 1q tended to occur in the posterior fossa of children and to behave aggressively. Our extensive data on ependymomas demonstrate significant associations between genetic aberrations and clinicopathological variables, and represent a starting point for further biological and clinical studies. British Journal of Cancer (2002) 86, 929–939. DOI: 10.1038/sj/bjc/6600180 www.bjcancer.com © 2002 Cancer Research UK Nature Publishing Group 2002-03-18 /pmc/articles/PMC2364143/ /pubmed/11953826 http://dx.doi.org/10.1038/sj.bjc.6600180 Text en Copyright © 2002 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Genetics and Genomics Carter, M Nicholson, J Ross, F Crolla, J Allibone, R Balaji, V Perry, R Walker, D Gilbertson, R Ellison, D Genetic abnormalities detected in ependymomas by comparative genomic hybridisation |
title | Genetic abnormalities detected in ependymomas by comparative genomic hybridisation |
title_full | Genetic abnormalities detected in ependymomas by comparative genomic hybridisation |
title_fullStr | Genetic abnormalities detected in ependymomas by comparative genomic hybridisation |
title_full_unstemmed | Genetic abnormalities detected in ependymomas by comparative genomic hybridisation |
title_short | Genetic abnormalities detected in ependymomas by comparative genomic hybridisation |
title_sort | genetic abnormalities detected in ependymomas by comparative genomic hybridisation |
topic | Genetics and Genomics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364143/ https://www.ncbi.nlm.nih.gov/pubmed/11953826 http://dx.doi.org/10.1038/sj.bjc.6600180 |
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