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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...

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Detalles Bibliográficos
Autores principales: Carter, M, Nicholson, J, Ross, F, Crolla, J, Allibone, R, Balaji, V, Perry, R, Walker, D, Gilbertson, R, Ellison, D
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2002
Materias:
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
Descripción
Sumario: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