Cytogenetic detection of unbalanced genomic aberrations in tumours is a strategy for the identification of tumour suppressor genes and oncogenes. When considered in concert with clinical data, the approach also represents a means of identifying markers of prognosis. In a preliminary investigation of the molecular basis of canine meningioma tumorigenesis, we profiled three tumours by comparative genomic hybridization. Distinct patterns of sub-chromosomal deletions were identified suggesting alternative mechanisms of tumour initiation. The deleted chromosomal segments encompass two regions (10q23.1 and 17q22-q23) that are syntenic to the chromosomes (22 and 1p) most often deleted in human meningiomas. A number of genes associated with DNA repair, cell cycle progression and apoptosis are located on both the deleted canine chromosomal segments and the syntenic regions deleted in human meningiomas. This study represents the first report of chromosomal copy number abnormalities in non-cultured canine brain tumour tissue.