(i) BZA, RLZ, and LAS inhibited the proliferation of breast cancer cells induced by CE, with the following antagonist power: BZA > RLX > LAS (ii) BZA inhibited a group of genes regulated by CE; this profile is different from those of RLX and LAS
(i) The stimulating effects of CE on the expression of amphiregulin (a marker of ductal proliferation) were antagonized by BZA > RLX > LAS (ii) BZA was more effective than RLX and LAS in reducing ductal growth
(i) 6-month treatment with BZA/CE significantly reduced the increase in epithelial density, the growth, and the ductal proliferation induced by CE (all ) (ii) BZA/CE treatment reduced ER protein expression and activity markers
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