[Hopeful]

Nguyen,

I think I can answer your question. Fulvestrant has a different method of action than the other hormonals. SERMs, like Tamoxifen, use a weaker estrogen than the body's own to bind to the estrogen receptors on the cells. AI's prevent the body from transforming androgens into ER, and thereby also deprive the ER receptors on the cells surfaces from binding ER circulating in the body. In contrast, Fulvestrant irreversibly erodes the ER receptors on the cells surface, so that ER is unable to bind to the cells. If you are giving high doses of ER as therapy, the therapy will only work if there are receptors on the cells for it to bind to. Since not all of the cells with ER receptors regenerate quickly, my assumption is that the researchers running the study wanted to assure themselves that the patients in the study had estrogen receptors on the cells for the estrogen therapy to bind to. Otherwise, it wouldn't work.

Hopeful