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Purpose: To examine benign orbital tumours for chromosomal imbalances. Methods : Specimens obtained from orbital tumours were screened for chromosomal imbalanc es using high resolution comparative genomic hybridization (CGH). The imbalances detected by CGH were confirmed by using fluorescence in situ hybridization (FIS H) and loss of heterozygosity (LOH) analysis. Results: Chromosomal gains or loss es were seen in 4/6 pleomorphic adenomas (gains at 8q; losses at 4p, 5p, 8p, 11p and 14q), 2/4 schwannomas (losses at 16p and 22q), and 1/9 cavernous haemangiom as (losses at 13q). Compared to previous studies of pleomorphic adenomas using G -band analysis, chromosomal imbalanceswere more frequently detected by using CG H. Gains of 8q11-q22 and losses of 4p15-pter, 11p12-p15, and 14q12-q23 in pl eomorphic adenomas, losses of 16p12-p13 in schwannomas, and losses of 13q32-qt er in cavernous haemangiomas have not been reported previously. Conclusions: A r ange of chromosomal imbalances was detected even within tumours of the same hist ological subtype. We did not observe common chromosomal gains or losses that wer e characteristic for orbital presentation of the tumours. The clinical relevance of the abnormalities is uncertain,but they may indicate the position of genes t hat could play a role in tumour development.
Methods: Specimens obtained from orbital toms were screened for chromosomal imbalanc es using high resolution comparative genomic hybridization (CGH). The imbalances detected by CGH were confirmed by using fluorescence in situ hybridization (FIS H ) and loss of heterozygosity (LOH) analysis. Results: Chromosomal gains or loss es were seen in 4/6 pleomorphic adenomas (gains at 8q; losses at 4p, 5p, 8p, 11p and 14q), 2/4 schwannomas Compared to previous studies of pleomorphic adenomas using G-band analysis, chromosomal imbalanceswere more frequently detected by using CG H. Gains of 8q11-q22 and losses of 4p15 -pter, 11p12-p15, and 14q12-q23 in pl eomorphic adenomas, losses of 16p12-p13 in schwannomas, and losses of 13q32-qt er in cavernous haemangiomas have not been reported previously. Conclusions: Argege of chromosomal imbalances was dete cted even within tumors of the same histological subtype. We did not observe common chromosomal gains or losses that wer e characteristic for orbital presentation of the tumors. The clinical relevance of the abnormalities is uncertain, but they may indicate the position of genes t hat could play a role in tumour development.