We showed that I3C causes dose-dependent inhibition of estradiol (E2)-stimulated ER-α activity in cervical and breast cancer cells, by the use of an E2-responsive reporter (ERE-TK-Luc) and by testing the effect of I3C on expression of endogenous E2-responsive genes (Meng et al, 2000b). Here, TKT is linked to breast carcinoma.