Introduction

PR antagonists are a potential new therapeutic strategy for the treatment ofpatients with invasive BC. One such progesterone antagonist is Onapristone (ZK98.299) (1, 2). Onapristone was reported to have strong anti-progestational and anti-tumor activity. In the MXT mammary tumor model in mice, and the DMBA- and NMU-induced rat mammary tumors, the anti-tumor activity ofOnapristone was equal to or even greater than that of tamoxifen and oophorectomy (3, 4). Furthermore, in the Onapristone treated tumors differentiation of mitotically active polygonal tumor cells towards dysplastic glandular structures was noted. This was accompanied by a massive sequestering of secretory products (5). Morphometric data oftumor tissues indicated that apoptotic cell death is enhanced by Onapristone treatment (5). Additionally, tumor cells were found to accumulate in phase of the cell cycle following Onapristone treatment, with an accompanying significant and biologically relevant reduction in the number of cells in G2M and S phases, using flow cytometry (3). Thus, the accumulation of cells in may result from the induction ofdifferentiation. Although, mechanisms by which Onapristone exerts its effects have been suggested, it is not known which genes are affected by the drug treatment in BC cells. The aim of this study was to identify genes which are affected by Onapristone in-vitro using microarray technology.

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