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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 prevention of breast cancer.
Here we're now going to consider the evolution of the use of
non-steroidal antioestrogens 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 at
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, oestradiol was not known to be the main sex steroid and 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
with 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 non-steroidal antioestrogens,
tamoxifen, in women without any disease.
But in 1985, when these ideas were developing,
if oestrogen is good for women's health to
protect from coronary heart disease and osteoporosis,
an antioestrogen could prevent breast cancer,
but could do harm.
It would be no use preventing breast cancer in
the few women that would have 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%.
So, the majority would have side effects.
No good if these women actually had coronary heart disease,
heart attacks, and crushing osteoporosis.