Endocrine therapy in breast and prostate cancer: SERMs, aromatase inhibitors and androgen deprivation
How tamoxifen, aromatase inhibitors, fulvestrant, GnRH agonists and antagonists, abiraterone and androgen receptor inhibitors work, why their mechanisms explain flare, mineralocorticoid excess, bone loss and drug interactions, and how resistance develops.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- About 70% of breast cancers are oestrogen receptor-positive. Endocrine therapy works by removing oestrogen or blocking its receptor.
- Almost all prostate cancers depend on androgen receptor signalling at diagnosis. Androgen deprivation therapy (ADT) removes testicular testosterone; newer agents block adrenal and intratumoural androgen synthesis or the receptor itself.
- Most adverse effects are the predictable result of hormone loss: hot flushes, bone loss, arthralgia, metabolic change.
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Sources
- eviQ cancer treatments onlineAU/NZCancer Institute NSW, 2026
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- Elacestrant Public Summary Document, March 2025 PBAC meetingAU/NZPharmaceutical Benefits Advisory Committee, 2025
- Elacestrant (Orserdu) medicine status, July 2026 PBAC meetingAU/NZPharmaceutical Benefits Scheme, 2026
- ESMO metastatic breast cancer living guidelineEuropean Society for Medical Oncology, 2025
- EAU-EANM-ESTRO-ESUR-ISUP-SIOG Guidelines on Prostate CancerEuropean Association of Urology, 2025
- Goodman & Gilman's The Pharmacological Basis of Therapeutics (14th ed.)McGraw Hill (Brunton and Knollmann, 2023), 2023
- Last updated
- 14 November 2026
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