Comparative genomic hybridization (CGH) to metaphase chromosome targets (1 ,2 ) has significantly contributed to our understanding of the cancer cytogenetics of more complex malignancies such as solid tumors (3 ,4 ). This molecular cytogenetics-based technique (hereafter referred to as “chromosome CGH”) is capable of defining genome-wide DNA copy number imbalances in sample cells relative to a normal reference in a single experiment. Chromosome CGH has greatly increased our understanding of tumor biology and progression since the minimal recurrent regions of chromosomal gain and loss are likely to contain novel oncogene(s) and tumor suppressor gene(s) respectively.