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Gain of 1q and loss of 22 are the most common changes detected by comparative genomic hybridisation in paediatric ependymoma
Author(s) -
Ward Samantha,
Harding Brian,
Wilkins Peter,
Harkness William,
Hayward Richard,
Darling John L.,
Thomas David G.T.,
Warr Tracy
Publication year - 2001
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.1167
Subject(s) - ependymoma , biology , comparative genomic hybridization , chromosome , population , incidence (geometry) , cytogenetics , genetics , pathology , gene , medicine , physics , environmental health , optics
Ependymomas are the third most common brain tumour in the paediatric population. Although cytogenetic and molecular analyses have pinpointed deletions of chromosomes 6q, 17, and 22 in a subset of tumours, definitive patterns of genetic aberrations have not been determined. In the present study, we analysed 40 ependymomas from paediatric patients for genomic loss or gain using comparative genomic hybridisation (CGH). Eighteen of the tumours (45%) had no detectable regions of imbalance. In the remaining cases, the most common copy number aberrations were loss of 22 (25% of tumours) and gain of 1q (20%). Three regions of high copy number amplification were noted at 1q24‐31 (three cases), 8q21‐23 (two cases), and 9p (one case). Although there was no association with the loss or gain of any chromosome arm or with benign versus anaplastic histologic characteristics, the incidence of gain of 7q and 9p and loss of 17 and 22 was significantly higher in recurrent versus primary tumours. This study has identified a number of chromosomal regions that may contain candidate genes involved in the development of different subgroups of ependymoma. © 2001 Wiley‐Liss, Inc.