Spectrum of copy number changes in low grade paediatric brain tumours detected by comparative genomic hybdidisation
Warr, Tracy Ward, Samantha Idowu, Michael O. Gregory, S. Darling, John L. Thomas, David G.
Warr, Tracy
Ward, Samantha
Idowu, Michael O.
Gregory, S.
Darling, John L.
Thomas, David G.
Editors
Other contributors
Affiliation
Epub Date
Issue Date
2001
Submitted date
Alternative
In: Abstracts from the 14th International Conference on Brain Tumor Research and Therapy. Asheville, North Carolina, USA. May 27-30, 2001. No.180
Abstract
Several different types of low-grade brain tumours arise predominantly in the paediatric population, including astrocytoma, craniopharygioma and choroid plexus papilloma (CPP). As yet, the genetic events that contribute to their development have not been well defined. We have used comparative genomic hybridisation (CGH) to identify regions of genetic loss and gain in a series of 30 low grade tumours comprising 7 pilocytic astrocytoma (WHO grade I), 12 grade II astrocytoma, 5 craniopharyngioma (WHO grade I) and 6 CPP (WHO grade I). In the group of astrocytoma, there were no detectable regions of genomic imbalance in all 7 grade I tumours and in 9 of 12 grade II tumours. The copy number changes in the remaining 3 cases of grade II astrocytoma were gain of 7p and 12p; loss of 1p, 12q and 22; gain of 2q, 3, 8q and 18q, respectively. Similarly, 4 of 5 craniopharyngioma appeared to have normal CGH profiles, although multiple changes including gain of 4, 6q, 8q and 18q and loss of 17, 20q and 22 were observed in the sixth case. In contrast, copy number aberrations were detected in 3 of 6 CPP. In one tumour, gain of 7 was the sole change, whereas gain of 3q and 6q and loss of 9q and 21 were detected in a second case. However, in the remaining CPP all chromosomes except X and Y were involved in copy number changes with gain of 1, 7, 9, 12, 15, 16, 18, 20 and 22 and loss of the remaining autosomes. Overall, genomic imbalance was detected in only 7 of these low grade tumours and it was not possible to identify consistent regions of loss and gain. Considerably larger numbers of each tumour type need to be analysed in order to elucidate the genetic pathways involved in tumourigenesis.
Citation
Neuro-oncology, 3(Suppl 1): 310
Journal
Research Unit
PubMed ID
PubMed Central ID
Embedded videos
Additional Links
Type
Conference contribution
Language
en
Description
Abstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press.
Series/Report no.
ISSN
1522-8517