Comparative genome hybridization reveals specific genomic imbalances during the genesis from benign through borderline to malignant ovarian tumors

Ovarian cancer is one of the most common types of malignancy in women throughout the developed world. Despite recent therapeutic advances, long-term survival is poor because ovarian cancer is largely asymptomatic in its early stages. Comparative genomic hybridization (CGH) was applied to a series of 8 benign, 8 borderline, and 17 malignant ovarian to establish genomic imbalances associated with tumor progression. Benign and borderline tumors were characterized by losses at 1p32∼p11, 2q14∼q34, 4q13∼q34, 5q11∼q23, and 6q12∼q24, as well as gains of 6p and chromosome 12. Similar chromosomal changes were also detected in malignant tumors but included additional chromosomal changes: gains at 1q21∼q31, 2p, 3q, 5p, 7, 10p, 12p, 16p, 17, 19q, 20q, and 22q, as well as losses at X, 3p, 8p, 9, 11p, 13, 14, and 18. Some individual cases of benign and borderline tumors revealed no genetic alterations detectable by CGH, suggesting that these tumors may represent a subset of tumors that originate by an alternative mechanism of tumorigenesis. Furthermore, our findings reveal that borderline tumors are more similar to benign tumors than to malignant tumors with respect to their genetic profiles.