Androgen deprivation therapy (ADT)
Androgen deprivation therapy (ADT) lowers the level of androgens — male sex hormones, mainly testosterone — or blocks their action, because prostate cancer cells need androgens to grow. Almost all of the body's testosterone is produced in the testicles, so treatment aims chiefly at shutting down this source, either with drugs or by surgical removal of the testicles (orchiectomy). ADT is used in high-risk early prostate cancer alongside radiotherapy, after recurrence, and in metastatic disease, often combined with newer hormonal drugs or chemotherapy.
How it works
Androgens drive the growth of both normal and cancerous prostate cells: they bind to the androgen receptor, which then switches on genes that make the cells divide. ADT interrupts this process in one of three ways — by stopping the testicles from producing androgens (GnRH agonists or antagonists, or orchiectomy, known as medical or surgical castration), by blocking the androgen receptor with antiandrogens (such as bicalutamide or the newer enzalutamide, apalutamide, and darolutamide), or by inhibiting androgen synthesis throughout the body (abiraterone).
The effects on the whole body are significant: lowered libido, erectile dysfunction, hot flashes, loss of bone density and muscle mass, weight gain, and mood changes; the risk of side effects increases the longer treatment lasts. Over time some cancers learn to grow despite very low testosterone levels — this is called castration-resistant prostate cancer and requires other forms of treatment.
Used in
Prostate
C61
foundation of systemic treatment in advanced and metastatic disease