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Metastatic prostate cancer — castration-sensitive and castration-resistant
In metastatic prostate cancer the androgen axis is blocked at two levels — testosterone suppression (ADT) and a novel androgen receptor drug — with docetaxel added in high-volume disease; once the disease becomes castration-resistant you move to chemotherapy, PARP inhibitors or radioligand therapy by biology.
Why it matters in the exam
Metastatic prostate cancer appears in the exam every year, in both the radiation and the systemic parts. Stems show a man with bone metastases and ask about treatment in the hormone-sensitive phase, when to add docetaxel, who gains from radiation to the prostate itself and the mechanism of castration resistance.
Further questions cover the mechanism and side effects of abiraterone and enzalutamide, preparation for denosumab, genomic changes on NGS that predict response to PARP inhibitors, and recognising aggressive-variant prostate cancer that needs platinum-based chemotherapy. Spinal cord compression from a vertebral metastasis is also a recurring scenario.
Key points
- In the hormone-sensitive phase every patient gets ADT with a novel androgen receptor drug, not ADT alone.
- In high volume add docetaxel, and in low volume add prostate radiation, which prolongs survival.
- Castration resistance is progression despite testosterone below 50 ng/dL, usually through the receptor itself.
- In castration resistance treatment is chosen by what was already given and by NGS: docetaxel, cabazitaxel, PARP inhibitors or lutetium-177 PSMA.
- Key effects: abiraterone — mineralocorticoid excess and liver injury; enzalutamide — fatigue and seizures; denosumab — hypocalcaemia and jaw osteonecrosis.
Summary table
| Situation | Treatment | Exam detail |
|---|---|---|
| Metastatic hormone-sensitive, low volume | ADT with an androgen receptor drug, plus radiation to the prostate | Prostate radiation prolonged survival only in low volume |
| Metastatic hormone-sensitive, high volume | ADT with an androgen receptor drug and docetaxel (triplet) | High volume: visceral metastases, or 4 or more bone metastases with at least one outside the spine and pelvis |
| Starting ADT with a GnRH agonist | Add an anti-androgen in the first weeks, or use an antagonist (degarelix, relugolix) | A transient testosterone rise (flare) may worsen pain or cord compression |
| Castration-resistant (testosterone below 50 ng/dL with progression) | An androgen receptor drug not yet given, docetaxel, then cabazitaxel | Resistance mechanisms: receptor amplification, receptor mutations, the AR-V7 variant and androgen production within the tumour |
| BRCA1, BRCA2 or ATM mutation | PARP inhibitor (olaparib), alone or with a receptor drug | Germline and somatic testing for every metastatic patient |
| PSMA-positive on PET after exhausting treatments | Lutetium-177 PSMA | Radium-223 only for symptomatic bone metastases without visceral metastases |
| Aggressive variant | Platinum-based chemotherapy | Visceral metastases, lytic bone metastases, low PSA relative to burden, neuroendocrine features |
In the full version for subscribers
- A simple algorithm
- Memory aid
- Exam traps
- 5 review cards
- Enough for IMLE
The full version is open to subscribers of: Oncology, Urology, Medical licensing exam (IMLE).
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Sources
- NCCN Clinical Practice Guidelines in Oncology: Prostate Cancer, 2026 — Systemic therapy for metastatic castration-sensitive and castration-resistant disease
- ESMO Clinical Practice Guideline: Prostate cancer, 2020, updated 2025 — Management of advanced disease
- DeVita, Hellman and Rosenberg's Cancer: Principles and Practice of Oncology, 12th ed. (2023) — Cancer of the prostate
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.