The treatment of breast cancer in the early 1960s was primarily limited to chemotherapy. While such agents are very effective, they do also have a significant number of side effects—many of which are related to the fact that they are active against fast-growing cells. Thus, fast-growing cells other than cancer cells may be incidental targets for these toxic drugs, particularly cells of the hair follicles, bone marrow, and gastrointestinal tract. This fact triggered interest in alternative and less toxic therapies for breast cancer.
By the 1960s it had become evident that at least some forms of breast cancer were dependent on hormones for growth, specifically on the steroid hormone estrogen. Evidence for this association originated almost a century ago, with the observation that in some women surgical ovariectomy (removal of the ovaries) caused shrinkage or remission of breast cancers. Much later evidence showed that some types of breast cancer were dependent on estrogen for growth. With removal of the ovaries—the primary source of estrogen in women—estrogen levels were reduced, causing inhibition of breast cancer cell growth. Agents that blocked the effects of estrogen proved to be equally effective in the treatment of estrogen-receptor-positive breast cancer.