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Analysis of ependymomas using comparative genomic hybridisation

Analysis of ependymomas using comparative genomic hybridisation
Analysis of ependymomas using comparative genomic hybridisation
Background and objectives Ependymomas are the third most common CNS tumours in childhood, and account for 9–12% of CNS neoplasms in all age groups. However, the prognosis for cases not completely excised is poor and the underlying biology of their development and progression is poorly understood. The few studies published to date have suggested that specific chromosomal abnormalities may be associated with the development of a significant proportion of these tumours. We setout to screen a large series of intracranial and spinal ependymomas for genetic imbalances, and to correlate these with histology and clinical behaviour.
Methods Comparative genomic hybridisation (CGH) was used to detect chromosome imbalances on 86 ependymomas from 77 patients, of which 22 were children under 16, treated at one of three UK centres (Newcastle, Nottingham, Southampton). Cases were first analysed without reference to histology or clinical features, and were then divided up according to anatomical location, histology and age at presentation.
Results Chromosomal imbalances were detected in tumours from 63/77 patients (82%). The majority involved entire chromosomes or chromosome arms, many showing patterns of gains suggestive of intermediate ploidy. Of previously reported abnormalities in ependymoma, the most frequent findings were gain of 1 q, seen in 13 cases (17%), and loss of 22 in 20 (26%). Whereas 1 q gain was seen mainly in posterior fossa tumours and was restricted to those with classic and anaplastic histology, loss of 22 was rarely observed in tumours from this location and their histology was predominantly classic or myxopapillary. In contrast to previous studies, loss of 6q was found in only 6 cases (8%) and in only one child. Out of 7 tumours biopsied at presentation and relapse, 4 revealed imbalances and 3 of these demonstrated progression of abnormalities at relapse.
Conclusions Chromosomal imbalance is common in ependymoma and patterns of abnormality are emerging that are associated with histology or location. Further studies are needed to establish the prognostic significance of these abnormalities.
analysis, england, scotland, time, ependymoma
0007-0920
p.108
Carter, M.
99ed122b-ea4c-4fc4-a83a-8a4a1c3aa729
Ross, F.M.
ec0958f8-b992-4e4a-b7e3-c474600390ba
Nicholson, J.C.
3d33321d-091d-41fc-b070-9f0def974e6d
Allibone, R.
b2353fa1-20ad-44ca-813d-5127c1f5d52f
Balaji, V.
545789cb-fe71-4c59-a675-aa882b76abf3
Crolla, J.A.
c5f23751-8de9-4a55-9cc5-ca2fb635769c
Gilbertson, R.J.
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Perry, R.H.
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Walker, D.A.
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Ellison, D.W.
5c53c9e1-ba51-425a-9bbd-14b1981272f1
Carter, M.
99ed122b-ea4c-4fc4-a83a-8a4a1c3aa729
Ross, F.M.
ec0958f8-b992-4e4a-b7e3-c474600390ba
Nicholson, J.C.
3d33321d-091d-41fc-b070-9f0def974e6d
Allibone, R.
b2353fa1-20ad-44ca-813d-5127c1f5d52f
Balaji, V.
545789cb-fe71-4c59-a675-aa882b76abf3
Crolla, J.A.
c5f23751-8de9-4a55-9cc5-ca2fb635769c
Gilbertson, R.J.
7aa864b8-301d-4c88-a9aa-e236b940371c
Perry, R.H.
a41f1d70-8538-47aa-ae4a-92b8a3fa1f94
Walker, D.A.
4fc726f1-d011-4ca7-8b9a-47f7c3a28734
Ellison, D.W.
5c53c9e1-ba51-425a-9bbd-14b1981272f1

Carter, M., Ross, F.M., Nicholson, J.C., Allibone, R., Balaji, V., Crolla, J.A., Gilbertson, R.J., Perry, R.H., Walker, D.A. and Ellison, D.W. (2001) Analysis of ependymomas using comparative genomic hybridisation. British Journal of Cancer, 85 (S1), p.108. (doi:10.1054/bjoc.2001.1918).

Record type: Article

Abstract

Background and objectives Ependymomas are the third most common CNS tumours in childhood, and account for 9–12% of CNS neoplasms in all age groups. However, the prognosis for cases not completely excised is poor and the underlying biology of their development and progression is poorly understood. The few studies published to date have suggested that specific chromosomal abnormalities may be associated with the development of a significant proportion of these tumours. We setout to screen a large series of intracranial and spinal ependymomas for genetic imbalances, and to correlate these with histology and clinical behaviour.
Methods Comparative genomic hybridisation (CGH) was used to detect chromosome imbalances on 86 ependymomas from 77 patients, of which 22 were children under 16, treated at one of three UK centres (Newcastle, Nottingham, Southampton). Cases were first analysed without reference to histology or clinical features, and were then divided up according to anatomical location, histology and age at presentation.
Results Chromosomal imbalances were detected in tumours from 63/77 patients (82%). The majority involved entire chromosomes or chromosome arms, many showing patterns of gains suggestive of intermediate ploidy. Of previously reported abnormalities in ependymoma, the most frequent findings were gain of 1 q, seen in 13 cases (17%), and loss of 22 in 20 (26%). Whereas 1 q gain was seen mainly in posterior fossa tumours and was restricted to those with classic and anaplastic histology, loss of 22 was rarely observed in tumours from this location and their histology was predominantly classic or myxopapillary. In contrast to previous studies, loss of 6q was found in only 6 cases (8%) and in only one child. Out of 7 tumours biopsied at presentation and relapse, 4 revealed imbalances and 3 of these demonstrated progression of abnormalities at relapse.
Conclusions Chromosomal imbalance is common in ependymoma and patterns of abnormality are emerging that are associated with histology or location. Further studies are needed to establish the prognostic significance of these abnormalities.

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More information

Published date: 31 July 2001
Additional Information: British Cancer Research Meeting 2001, poster presentation P293
Keywords: analysis, england, scotland, time, ependymoma

Identifiers

Local EPrints ID: 59554
URI: http://eprints.soton.ac.uk/id/eprint/59554
ISSN: 0007-0920
PURE UUID: 6cb4a576-4287-4713-9114-47c0efdffa56

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Date deposited: 03 Sep 2008
Last modified: 15 Mar 2024 11:16

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Contributors

Author: M. Carter
Author: F.M. Ross
Author: J.C. Nicholson
Author: R. Allibone
Author: V. Balaji
Author: J.A. Crolla
Author: R.J. Gilbertson
Author: R.H. Perry
Author: D.A. Walker
Author: D.W. Ellison

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