Comparison of alterations of chromosome 17 in carcinoma of the ovary and of the breast

Breast and ovarian carcinomas share a region of allelic loss on chromosome 17q25, suggesting that these tumours may arise by similar molecular pathway s. We analysed paraffin-embedded tissues from 84 sporadic ovarian carcinoma s and 42 sporadic infiltrating ductal carcinomas of the breast for abnormal ities on chromosome 17. Loss of heterozygosity (LOH) of at least one inform ative marker on 17q was identified in 49 of 82 (60%) ovarian carcinomas, as against only 6 of 40 (15%) informative breast carcinomas (P<0.0001). In ov arian carcinoma, LOH was most commonly observed for GH on 17q23 (56%), and was also frequently observed at 17q21 (46%). In contrast, LOH of D17S1330/C TT16 on 17q25 was observed in only 19% of ovarian tumours. LOH in breast ca rcinomas was most frequently observed at 17q21 (16%), less frequently at 17 q23 (7%) and not identified at all at 17q25 in any breast cancers. Immunohi stochemical analysis demonstrated overexpression of the p53 gene product in 38 of 84 (45%) ovarian carcinomas, as against 10 of 42 (24%) breast carcin omas (P=0.0195), p53 immunoreactivity was significantly associated with LOH in ovarian and breast cancers. Immunohistochemical expression of HER2/neu was observed in 6 of 84 (7%) ovarian and 3 of 42 (7%) breast carcinomas. Th ere was no relationship between HER2/neu immunoreactivity and LOH. Although sporadic carcinomas of breast and ovary share some regions of allelic loss on chromosome 17q, differences in other alterations on this chromosome sug gest divergent pathways of tumour development.