Coradini D, Biffi A, Pirronello E, Di Fronzo G
Divisione di Oncologia Sperimentale C, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy.
Anticancer Res. 1995 Mar-Apr;15(2):315-9.
The presence of steroid receptors in breast cancer is usually considered as a good indicator for responsiveness to antiestrogen treatment. However, not all estrogen-receptor (ER) positive tumors respond to tamoxifen, probably owing to the natural heterogeneity of breast cancer, which after tamoxifen treatment can result in an overgrowth of selected ER-negative clones. Since in a previous study we found that beta-interferon exerts an antiproliferative activity on several breast cancer cell lines, regardless of their steroid receptor status, we addressed our attention to the possibility of improving tamoifen efficacy by the addition of beta-interferon. Thus, we investigated the effect of concomitant or sequential treatment with tamoxifen and beta-interferon on breast cancer cell lines (MCF7, T47D, MDA-MB231, BT20) characterized by a different steroid receptor status. The results showed that beta-interferon caused a cell growth inhibition additional to that produced by tamoxifen, regardless of the receptor status of the cell lines. These findings indicate the potential of the combined treatment with tamoxifen and beta-interferon due to the direct effect of beta-interferon on ER-negative cells and the potentiation of tamoxifen activity in ER-positive cells, perhaps through the induction of steroid receptor synthesis.