Hormonal therapy of cancer: breast, prostate, neuroendocrine and thyroid tumours

Some cancers grow on hormones. Removing the hormone or blocking its receptor slows them, often for years.

Updated Nov 12, 2026

Certain tumours keep the hormone dependence of the tissue they came from: breast cancers with oestrogen or progesterone receptors, prostate cancers driven by androgens, neuroendocrine tumours with somatostatin receptors, and well-differentiated thyroid cancers that respond to TSH. Endocrine therapy either lowers the hormone, blocks its receptor or destroys the receptor. Receptor testing on the tumour decides who benefits.

Key points

Hormone receptor testing (ER, PR) on breast tumour tissue decides who receives endocrine therapy.
Breast strategies: stop ovarian oestrogen (GnRH agonists, oophorectomy), block peripheral oestrogen synthesis (aromatase inhibitors), or block or degrade the receptor (tamoxifen, fulvestrant).
Aromatase inhibitors are used after menopause, or before menopause only together with ovarian suppression.
Prostate cancer is treated with androgen deprivation therapy (ADT); GnRH agonists cause an initial testosterone flare, antagonists do not.
Most prostate cancers eventually become castration resistant, yet still respond to newer androgen-pathway drugs such as abiraterone and enzalutamide.
Somatostatin analogues control symptoms and growth of some neuroendocrine tumours; TSH suppression with levothyroxine supports surgery and radioiodine in differentiated thyroid cancer.

Principles: receptor status and hormone dependence

A hormone-dependent tumour uses a hormone receptor as a growth switch. Endocrine therapy works only if the receptor is present and still drives growth, which is why the receptor is measured in tumour tissue before treatment. These drugs are generally less toxic than chemotherapy but are taken for years, and their side effects are those of hormone deficiency. Over time tumours can escape, for example through receptor mutations, receptor amplification or new growth pathways, which leads to sequencing of agents and combinations with targeted drugs such as CDK4/6 inhibitors.

Breast cancer

Ovarian suppression: GnRH agonists (goserelin, leuprorelin) or surgical removal or radiation of the ovaries, used in premenopausal women.
Aromatase inhibitors (anastrozole, letrozole, exemestane) block conversion of androgens to oestrogen in fat and other tissues; they lower oestrogen after menopause.
SERMs: tamoxifen blocks the receptor in breast tissue but acts like oestrogen in the uterus and on clotting, so it raises the risk of endometrial cancer and venous thrombosis.
SERDs: fulvestrant (and the oral elacestrant) bind the receptor and lead to its destruction.
Adjuvant endocrine therapy is usually continued for years, sometimes switching from tamoxifen to an aromatase inhibitor.
Progestins (medroxyprogesterone, megestrol) are mainly used in endometrial cancer.
Drugs that inhibit CYP2D6, such as some antidepressants, may reduce tamoxifen activity, because CYP2D6 helps form its active metabolites.

Prostate cancer and androgen deprivation therapy

Testosterone and dihydrotestosterone drive both normal and malignant prostate cells. ADT lowers androgens to castrate levels by orchiectomy or, reversibly, with drugs.

GnRH (LHRH) agonists (leuprorelin, goserelin, triptorelin): first stimulate, then shut down pituitary LH release; the early testosterone surge (flare) can worsen bone pain or urinary obstruction, so an antiandrogen is often given for the first weeks.
GnRH antagonists (degarelix, relugolix): block the pituitary receptor directly, with no flare.
Androgen receptor blockers (bicalutamide, enzalutamide, flutamide): compete with androgens at the receptor; usually combined with ADT.
Androgen synthesis inhibitor: abiraterone blocks CYP17 in testes, adrenal glands and tumour; it is given with prednisone to prevent mineralocorticoid excess.

Castration resistance and ADT side effects

Early tumours are castration sensitive. Most eventually grow despite castrate testosterone levels (castration-resistant prostate cancer), often because the androgen receptor becomes amplified, mutated or activated by androgens the tumour makes itself. ADT is usually continued while abiraterone, enzalutamide, chemotherapy, radiopharmaceuticals, PARP inhibitors (for DNA-repair mutations) or immunotherapy are added.

Hot flushes, fatigue, mood changes and loss of libido and erectile function
Bone loss and fractures; bisphosphonates or denosumab protect bone
Loss of muscle, weight gain, insulin resistance and lipid changes
Breast tissue growth; risks generally increase with longer treatment

Neuroendocrine and thyroid tumours

Neuroendocrine tumours of the gut and pancreas often carry somatostatin receptors. Somatostatin analogues (octreotide, lanreotide) reduce hormone secretion and relieve carcinoid syndrome (flushing, diarrhoea); lanreotide is also used to treat advanced gastroenteropancreatic neuroendocrine tumours.
Well-differentiated thyroid cancer grows in response to TSH. After surgery and radioiodine (sodium iodide I-131), levothyroxine is used to keep TSH low; over-replacement can cause arrhythmias and bone loss, so the lowest effective amount is sought.

Test yourself

Think of the answer, then tap the question to see it.

Why are aromatase inhibitors not used alone in premenopausal women with breast cancer?

Their ovaries still make large amounts of oestrogen; aromatase inhibitors work there only when combined with ovarian suppression.

Why is an antiandrogen often started with a GnRH agonist in prostate cancer?

GnRH agonists first raise testosterone (flare), which can worsen bone pain or obstruction; the antiandrogen blocks the receptor during that surge.

What does castration-resistant prostate cancer mean?

The cancer keeps growing even though testosterone is at castrate levels; androgen-pathway drugs such as abiraterone or enzalutamide may still work.

Why does tamoxifen raise the risk of endometrial cancer while treating breast cancer?

As a SERM it blocks the oestrogen receptor in breast tissue but activates it in the uterus.

What is the purpose of levothyroxine after surgery for differentiated thyroid cancer?

Besides replacing hormone, it keeps TSH low, removing a growth signal for remaining TSH-dependent cancer cells.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: Hormone Therapy for Prostate Cancer (U.S. National Cancer Institute, 2026); Lanreotide Injection: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2026); DailyMed - LEVOTHYROXINE SODIUM tablet (DailyMed (U.S. National Library of Medicine), 2026).

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