(i) BZA blocked CE-induced stimulation, including DNA synthesis, reduction of apoptosis, expression of cMyc, pS2, and WNT1-inducible signaling pathway protein 2
(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) BZA blocked gene expression induced by CE and the growth of mammary terminal ducts and acini (ii) BZA blocked tumor growth and gene expression in mice with MCF-7 xenografts
(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