Platelet-derived growth factor expression in phyllodes tumors and fibroadenomas of the breast

The development of normal breast tissue and the pathogenesis of various tumors are influenced by growth factor-mediated epithelial-stromal interactions. Similar interactions may occur in fibroepithelial breast tumors. We have studied the expression of platelet-derived growth factor (PDGF) and PDGF beta receptor (PDGFR beta) in 46 phyllodes tumors (18 benign, 15 borderline, 13 malignant), 11 fibroadenomas, and 6 samples of normal breast. There was neoplastic stromal cell positivity for PDGFR beta in almost 50% of phyllodes tumors and for PDGF in 24%. Both were associated with prominent nuclear pleomorphism (P < .01), PDGF with high grade (P < .01), and a higher mean Ki-67 labeling index (P = .013), and PDGFR beta with conspicuous stromal overgrowth (P < .01). Go-positivity for stromal PDGF and PDGFR<beta> was found in 15% of phyllodes tumors, and for epithelial PDGF and stromal PDGFR beta in 43%. Both types of co-positivity were associated with prominent nuclear pleomorphism and the latter type with conspicuous stromal overgrowth (all P < .01). Follow-up of 41 phyllodes tumors showed that disease-related death was associated with established histologic features of malignancy including mitotic count, stromal overgrowth, an infiltrative tumor margin, and nuclear pleomorphism. In addition, stromal PDGFR<beta> positivity (P = .013) and epithelial PDGF/stromal PDGFR beta co-positivity (P = .0075) were associated with disease-related death. Stromal PDGF and PDGFR beta expression in fibroadenomas was less common and less extensive (P < .05) than in phyllodes tumors. The results suggest that PDGF influences the pathogenesis of fibroepithelial breast tumors and that PDGF-dependent paracrine and autocrine mechanisms may operate. Also, it is possible that assessment of PDGF and PDGFR<beta> expression could contribute to the management of these tumors in the future. HUM PATHOL 31:1214-1222. Copyright (C) 2000 by W.B. Saunders Company.