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Genetic abnormalities detected in ependymomas by comparative genomic hybridisation

Genetic abnormalities detected in ependymomas by comparative genomic hybridisation
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 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.
0007-0920
929 - 939
Carter, M.
99ed122b-ea4c-4fc4-a83a-8a4a1c3aa729
Nicholson, J.
bba232d3-f7fa-4a3f-b409-1463eb19869f
Ross, F.
ec0958f8-b992-4e4a-b7e3-c474600390ba
Crolla, J.
c5f23751-8de9-4a55-9cc5-ca2fb635769c
Allibone, R.
b2353fa1-20ad-44ca-813d-5127c1f5d52f
Balaji, V.
545789cb-fe71-4c59-a675-aa882b76abf3
Perry, R.
40cdf881-b9da-4bac-a76a-89c6fcf156a5
Walker, D.
26d59048-0785-4861-9c83-4bae3c33caad
Gilbertson, R.
13c238c9-a213-4c22-baac-34378c48b033
Ellison, D. W.
80f2f07f-f454-43f8-b674-b5bfbe136ab7
Carter, M.
99ed122b-ea4c-4fc4-a83a-8a4a1c3aa729
Nicholson, J.
bba232d3-f7fa-4a3f-b409-1463eb19869f
Ross, F.
ec0958f8-b992-4e4a-b7e3-c474600390ba
Crolla, J.
c5f23751-8de9-4a55-9cc5-ca2fb635769c
Allibone, R.
b2353fa1-20ad-44ca-813d-5127c1f5d52f
Balaji, V.
545789cb-fe71-4c59-a675-aa882b76abf3
Perry, R.
40cdf881-b9da-4bac-a76a-89c6fcf156a5
Walker, D.
26d59048-0785-4861-9c83-4bae3c33caad
Gilbertson, R.
13c238c9-a213-4c22-baac-34378c48b033
Ellison, D. W.
80f2f07f-f454-43f8-b674-b5bfbe136ab7

Carter, M., Nicholson, J., Ross, F., Crolla, J., Allibone, R., Balaji, V., Perry, R., Walker, D., Gilbertson, R. and Ellison, D. W. (2002) Genetic abnormalities detected in ependymomas by comparative genomic hybridisation. British Journal of Cancer, 86 (6), 929 - 939. (doi:10.1038/sj/bjc/6600180).

Record type: Article

Abstract

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.

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Published date: 2002

Identifiers

Local EPrints ID: 24646
URI: http://eprints.soton.ac.uk/id/eprint/24646
ISSN: 0007-0920
PURE UUID: f41475e1-903a-406b-a8d8-3fd034cec364

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Date deposited: 04 Apr 2006
Last modified: 14 Sep 2021 20:25

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Contributors

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

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