While these compounds appear to have little or no effect on ERα/α homodimerization and transcriptional activation in HEK293 BRET and ERE-luciferase assays employing exogenous ERs (Fig. 3), treatment of breast and prostate cancer cells expressing ERα at a much higher level than ERβ (PC3-shERβ) results in ERα-dependent growth increases (Fig. 6E). The gene discussed is ESR2; the disease is prostate cancer.