Other Talks in the Series: The Cell Division Cycle

In the last lecture, we talked about tamoxifen, and the fact that tamoxifen was a failed contraceptive that
became the gold standard for the treatment and to prevention of breast cancer. Here we're now going to consider the evolution of the use of nonsteroidal antiestrogens into being Selective Estrogen Receptor Modulators. In lecture two, we're considering the SERM story, Selective Estrogen Receptor Modulators. A chemoprevention is not a new concept. It was Professor Antoine Lacassagne, who back in 1936 made this statement to the American Association for Cancer Research: "If one accepts the consideration of adenocarcinoma of the breast as a consequence of a special hereditary sensibility to the proliferative actions of oestrone." In those days, estrone was not known to be the main sex story or an activity, "one is led to imagine a therapeutic preventative for subjects predisposed by their heredity to this cancer." Lacassagne was talking about animal models, oophorectomy, preventing breast cancer, but a therapeutic preventative became a potential possibility. But the extensive use of tamoxifen in the clinical community and preclinical information that set the scene to move forward into clinical testing. Now, it was in the 1980s that the whole idea of chemoprevention of breast cancer really started to take off. This was using nonsteroidal antiestrogen, tamoxifen, in women without any disease. But in 1985, when these ideas were developing, if estrogen is good for women's health to protect from coronary heart disease and osteoporosis, and antiestrogen could prevent breast cancer. But it could do harm, it would be no use. Preventing breast cancer in the few women that wouldn't have been affected because of incidence, as in about four or five high risk women will develop breast cancer out of a thousand and you can cut that down by about 50 percent. So, the majority would have side effects.