Aromatase Inhibitor — Hormone Therapy for Breast Cancer

Aromatase inhibitors are a class of endocrine therapeutics that suppress oestrogen biosynthesis. In postmenopausal individuals, the ovaries cease oestrogen production, leaving peripheral tissues—such as adipose tissue, muscle, and the brain—as the primary sources of oestrogen. In these tissues, the cytochrome P450 aromatase enzyme converts circulating adrenal androgens into oestrone and oestradiol.

Aromatase inhibitors bind to and deactivate this enzyme, reducing plasma oestrogen concentrations by up to 95 percent. They are categorised into two distinct groups: non-steroidal inhibitors (such as anastrozole and letrozole), which bind reversibly to the enzyme's haem group, and steroidal inactivators (such as exemestane), which bind irreversibly as substrate analogues.

For individuals with hormone receptor-positive breast cancer, aromatase inhibitors significantly reduce the risk of tumour recurrence and improve overall survival. They are commonly prescribed for five to ten years following surgery, chemotherapy, or radiotherapy. Choosing and adhering to an aromatase inhibitor regimen is a pivotal decision that provides sustained protection against metastatic spread.

Before starting an aromatase inhibitor, the tumour tissue must be tested using immunohistochemistry to confirm that it expresses oestrogen receptors (ER) and progesterone receptors (PR). Baseline bone mineral density (DEXA) scans are essential before treatment, alongside routine blood lipid profiles, because lowered oestrogen accelerates bone thinning and alters cardiovascular markers.

Aromatase inhibitors are specifically indicated for oestrogen receptor-positive (ER+) and progesterone receptor-positive (PR+) breast cancers. They are standard care for postmenopausal women and can also be used in premenopausal women when combined with chemical ovarian suppression, such as LHRH agonists, to halt ovarian hormone production.

Aromatase inhibitors are used as adjuvant therapy after surgery to prevent recurrence, as neoadjuvant therapy to shrink tumours before operation, or as first-line treatment for metastatic ER-positive disease. In advanced settings, they are frequently paired with CDK4/6 inhibitors or targeted PI3K pathway inhibitors to enhance effectiveness and overcome endocrine resistance.