Estrogen-responsive breast cancer cells, such as MCF7 and T47D cells, express both estrogen receptor ER and ERß. Indole-3-carbinol (I3C) strongly down-regulated ER protein and transcript levels, without altering the level of ERß protein, in both cell lines. In cells transfected with the ER promoter linked to a luciferase gene reporter, I3C ablated ER promoter activity1-5. Dietary indole-3-carbinol prevents the development of estrogen-enhanced cancers including breast. Whereas estrogen increases the growth and survival of tumors, indole-3-carbinol causes growth arrest and increased apoptosis and ameliorates the effects of estrogen. In these findings best use indole-3-carbinol together with other nutrients (genistein) to achieve maximum benefits for cancer prevention. Investigator evaluated whether genistein, which is the major isoflavonoid in soy, would alter the ability of indole-3-carbinol/DIM to cause apoptosis and decrease expression driven by the estrogen receptor (ER)-alpha.