Breast cancer can be oestrogen-sensitive, so a treatment target for such types is to inhibit oestrogen.

In premenopausal women, selective oestrogen receptor modulators, more conveniently called SERMs, include tamoxifen. This particular medication acts as an oestrogen receptor antagonist at the breast but an oestrogen receptor agonist at the uterus, which is why it minority increases the risk of endometrial cancer.

In postmenopausal women, aromatase inhibitors are an option. These interrupt the production of oestrogen by suppressing the action of the enzyme aromatase. Anastrazole and letrozole are the names to know here; they’re non-steroidal, reversible binders of aromatase from the third generation of aromatase inhibitors.

Why are aromatase inhibitors less effective in premenopausal women? Premenopausal women have a large quantity of aromatase in the ovary. Note that ovarian aromatase is sensitive to changes in the gonadotropin LH, which is produced by the pituitary gland. If aromatase is suppressed with an aromatase inhibitor, gonadotropins increase in response, according to the usual feedback pattern, which stimulates more ovarian aromatase. This makes aromatase inhibitors less proficient at inhibiting oestrogen production in the ovary in such a group.

References

1. Fabian, C. J. (2007). The what, why and how of aromatase inhibitors: hormonal agents for treatment and prevention of breast cancer. International Journal of Clinical Practice, 61(12), 2051–2063. http://doi.org/10.1111/j.1742-1241.2007.01587.x