Course Content
Module 1 — Principles of Hormone Therapy in Oncology
Mechanism and Dosing Overview Aromatase Inhibitors (AIs): block the enzyme aromatase (CYP19A1), which converts androgens to estrogens in adipose and peripheral tissues. Examples: Anastrozole 1 mg orally daily, Letrozole 2.5 mg orally daily, Exemestane 25 mg orally daily. These are the preferred agents in postmenopausal women with estrogen receptor–positive breast cancer. Selective Estrogen Receptor Modulators (SERMs): such as Tamoxifen 20 mg orally daily — bind the estrogen receptor and act as antagonists in breast tissue but partial agonists in bone and endometrium. Selective Estrogen Receptor Degraders (SERDs): such as Fulvestrant 500 mg intramuscularly on days 0, 14, 28, then every 28 days thereafter — promote estrogen receptor degradation. CYP17 Inhibitors: Abiraterone acetate 1000 mg orally daily on an empty stomach plus Prednisone 5 mg orally twice daily — block the CYP17A1 enzyme, suppressing androgen synthesis in adrenal glands and tumors. Gonadotropin-Releasing Hormone (GnRH) Agonists and Antagonists: Leuprolide 7.5 mg subcutaneously every 4 weeks or depot every 3–6 months; Degarelix 240 mg subcutaneously loading dose, then 80 mg every 4 weeks; Relugolix 120 mg orally daily — suppress testosterone or estrogen production by downregulating or directly blocking pituitary gonadotropin release.
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Hormone Therapy for Cancer Patients: Mechanisms, Indications, and Clinical Practice

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.