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):

  • Breast — Estrogen/Progesterone receptor positive (ER/PR+).

  • Prostate — Androgen receptor positive (AR+).

  • Endometrial — Estrogen/progesterone dependent.

  • Selected others — Thyroid (TSH suppression), neuroendocrine tumors (somatostatin analogs).

Clinical strategies (how we block the axis):

  1. Hormone production suppression

    • Surgical: oophorectomy / orchiectomy.

    • Medical: Gonadotropin-Releasing Hormone (GnRH) agonists/antagonists → ↓ LH/FSH → ↓ estrogen/testosterone.

  2. Receptor blockade

    • Selective Estrogen Receptor Modulator (SERM): tamoxifen.

    • Anti-androgens: bicalutamide, enzalutamide, apalutamide, darolutamide.

  3. Synthesis inhibition

    • Aromatase Inhibitors: anastrozole, letrozole, exemestane.

    • CYP17A1 inhibitor: abiraterone (plus prednisone).

  4. Receptor degradation

    • Selective Estrogen Receptor Degrader (SERD): fulvestrant.

Pearls for practice:

  • Always confirm dependence (ER/PR, AR, or hormone-responsive features) before starting.

  • Synergy with radiotherapy: In prostate cancer, adding androgen deprivation to RT improves outcomes (e.g., long-term ADT for high-risk disease).

  • Don’t drift on autopilot: reassess benefit vs QoL every 6–12 months.

Common pitfalls:

  • Starting endocrine therapy without receptor confirmation.

  • Forgetting bone health and metabolic prevention when using strong anti-estrogen/anti-androgen regimens.

Next