Chromosomal deletions, associated with the loss of normal function of tumour suppressor genes, have been identified in a variety of both familial and sporadic human cancers. Although the molecular pathology of ovarian cancer is not understood, several studies have reported deletions in chromosome I7 in ovarian turnours. We have used I 3 restriction site polymorphic, microsatellite, and variable number tandem repeat markers t o make a detailed analysis of chromosome I7 deletions in I 2 benign and I 9 malignant ovarian tumours. Two benign and I I malignant tumours were informative for at least one marker on each arm of the chromosome. Loss of heterozygosity (LOH) was detected in both arms (by all informative markers) in 5 malignant turnours from four women (three with the disease at FIG0 stage la). In a further bilateral ovarian tumour a partial LOH affecting I7q22-q25 was present in one ovary only. By contrast to a number of previous studies, none of the I9 malignant and I 2 benign tumours showed ERBB2 ( 17q 12-22) amplification. The data presented show that the loss of a whole copy of chromosome I 7 is a frequent and relatively early event in the development of some ovarian cancers. This suggests the possible involvement of multiple chromosome 17 loci in the pathogenesis of ovarian cancer. Equally plausible is that the loss of a whole chromosome copy could be the product of chromosomal instabilities induced by loss of the normal allele of tumour suppressors, such as TP53, located on this chromosome.