Concept (what’s going on):
Some tumors are driven by hormones. Endocrine (hormone) therapy blocks the hormone signal or its receptor to slow or stop cancer growth. (NCCN 2025; ESMO 2024; ASCO 2023–2024)
Major hormone-driven cancers (clinically relevant):
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Breast — Estrogen/Progesterone receptor positive (ER/PR+).
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Prostate — Androgen receptor positive (AR+).
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Endometrial — Estrogen/progesterone dependent.
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Selected others — Thyroid (TSH suppression), neuroendocrine tumors (somatostatin analogs).
Clinical strategies (how we block the axis):
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Hormone production suppression
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Surgical: oophorectomy / orchiectomy.
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Medical: Gonadotropin-Releasing Hormone (GnRH) agonists/antagonists → ↓ LH/FSH → ↓ estrogen/testosterone.
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Receptor blockade
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Selective Estrogen Receptor Modulator (SERM): tamoxifen.
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Anti-androgens: bicalutamide, enzalutamide, apalutamide, darolutamide.
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Synthesis inhibition
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Aromatase Inhibitors: anastrozole, letrozole, exemestane.
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CYP17A1 inhibitor: abiraterone (plus prednisone).
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Receptor degradation
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Selective Estrogen Receptor Degrader (SERD): fulvestrant.
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Pearls for practice:
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Always confirm dependence (ER/PR, AR, or hormone-responsive features) before starting.
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Synergy with radiotherapy: In prostate cancer, adding androgen deprivation to RT improves outcomes (e.g., long-term ADT for high-risk disease).
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Don’t drift on autopilot: reassess benefit vs QoL every 6–12 months.
Common pitfalls:
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Starting endocrine therapy without receptor confirmation.
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Forgetting bone health and metabolic prevention when using strong anti-estrogen/anti-androgen regimens.