PTEN and breast carcinoma: The ER’s association with the PPREinhibited PPARγ’s ability to induce transcription asdemonstrated by cotreatment of MCF-7 breast cancer cells with both Rosi and 17ß-estradiol.This cotreatment inhibited the induction of PTEN protein that was observed byRosi stimulation alone [22].This is an important observation as it is appealing to postulate that thiscrosstalk, between PPARγ and ER, may significantly affect breast cancertherapeutics as well as lead the way to the discovery of future novel treatmenttherapies.