ЗДРУЖЕНИ САДРЖАЈ РЕЦЕПТОРА ЗА ЕСТРОГЕН И ПРОГЕСТЕРОН У ПРЕДВИЂАЊУ ОДГОВОРА НА ХЕМИОТЕРАПИЈУ И ХОРМОНСКУ ТЕРАПИЈУ У КАРЦИНОМУ ДОЈКЕ СА ПОВЕЋАНОМ ЕКСПРЕСИЈОМ РЕЦЕПТОРА ЗА ХУМАНИ ЕПИДЕРМАЛНИ ФАКТОР РАСТА ДВА

Abstract

The predictive value of Human Epidermal growth factor Receptor 2 (HER-2) on the response to chemotherapy and endocrine therapy in breast cancer patients has not yet been determined. The expression of other biomarkers in breast cancer can further influence the response to therapy. The aim of our study was to investigate if status of steroid receptors (SR) influenced the response to anthracycline-containing chemotherapy and tamoxifen in a group of HER-2 positive advanced breast cancer patients. Forty breast cancer patients, who were entered into the various prospective clinical trials conducted at the Institute of Oncology and Radiology of Serbia during their metastatic phase of disease, were involved into this analysis. Steroid receptors content were determined both by biochemical method and immunohistochemical (ICH) method, while HER-2 content were determined only by ICH method. Twelve out of 40 women were sequentially treated by anthracycline-containing chemotherapy and, always upon disease progression, with antiestrogen tamoxifen. The objective response to anthracycline therapy was obtained in 4 out of 12 patients (RR = 0.33, CI 95% = 0.05-0.61). In three of them the response to tamoxifen was noticed, as well. Of 8 anthracycline resistant patients in this group, 7 patients also had disease progression as best response to tamoxifen despite the fact that most of them (5 out of 7 tamoxifen resistant women) had positive SR status. Our results showed a trend (Fisher test, p = 0.06) that clinical response to anthracycline-containing chemotherapy might be of some predictive value for the response to subsequent tamoxifen therapy in HER-2 positive advanced breast cancer patients. However, these results were obtained on a small number of patients, so further investigation is warranted.

Keywords: breast cancer, HER-2 overexpression, response to systemic therapy