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Prostate (male reproductive system)

Prostate cancer

How hormonal therapy, PSA testing and biomarker-directed drugs shaped prostate cancer care, and how to read its survival figures.

5-year relative survival · United States, SEER 8 registries

67.68%→98.65%

1975 (observed value; first year in the table) to 2018 (observed value; last observed year in the table). Read these with the caveats under “Then and now”.Source

36 milestones, by decade

  • The 1966 Nobel Prize in Physiology or Medicine was awarded to Charles Huggins "for his discoveries concerning hormonal treatment of prostatic cancer". The prize page dates his work showing that hormones can affect the course of the disease to around 1940. A 1941 paper by Huggins and Hodges, titled 'Studies on prostatic cancer: I. The effect of castration, of estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate', was reprinted in the Journal of Urology in 2002.
  • A Federal Register notice records that the FDA's Center for Devices and Radiological Health approved the Hybritech Tandem-R PSA assay application on 25 February 1986, for the quantitative serial measurement of PSA in serum to aid in the prognosis and management of people with prostate cancer. A second notice records that on 25 August 1994 the Center approved a supplement changing the intended use of the manufacturer's Tandem-R, -E and -ERA PSA assays to include measurement of serum PSA with digital rectal examination as an aid in the detection of prostate cancer in men aged 50 years or older, with prostatic biopsy required for diagnosis. Both notices concern one manufacturer's assays.
  • In the SEER 8 series on the SEER Cancer Stat Facts page, the observed age-adjusted rate of new prostate cancer cases was 95.39 per 100,000 men in 1975, 224.93 in 1992 and 127.08 in 2023, while the age-adjusted US death rate was 30.94 per 100,000 in 1975, 39.88 in 1993 and 18.40 in 2024. The observed five-year relative survival in the same SEER 8 table was 67.68% in 1975 and 98.65% in 2018, and 89.71% already in 1990. The page does not say how much of the change reflects screening and earlier diagnosis, stage mix or treatment, and does not label the table's year as year of diagnosis.

Evidence current to October 2026 · Checked against primary sources to the extent possible

A guided tour of 12 milestones. You can pause or step through it yourself.

Filter milestonesshowing all 36
Treatment type
Setting

The age of rays

  1. 1905 · Treatment · SurgeryYoung's radical perineal prostatectomy for cancer (1904-05)In 1905 the Johns Hopkins surgeon Hugh Young described a radical operation through the perineum that removed the whole prostate, the seminal vesicles and part of the bladder, and he proposed it as a routine for prostate cancer. He reported four operations done since 1904; two of the four men had died by the time of the report.Young (1905) described a radical perineal prostatectomy removing prostate, seminal vesicles, parts of the vasa deferentia and a bladder cuff in one piece, with bladder-to-urethra anastomosis, proposed as a routine for prostate cancer, within a study of 40 cases. Four men were operated on in 1904-05. He reported no operative mortality; one man died six weeks after surgery after ureteral excision he called a mistake, and one died after later litholapaxy.
  2. 1941 · Treatment · EndocrineHuggins and Hodges: hormones and prostate cancer (1941)In 1941 Charles Huggins and Clarence Hodges published studies of men whose prostate cancer had spread, looking at how castration, estrogen and testosterone injections changed blood phosphatase levels. Huggins later shared the 1966 Nobel Prize in Physiology or Medicine for discoveries concerning hormonal treatment of prostatic cancer.Huggins and Hodges, Cancer Research 1941 (reprinted J Urol 2002): effect of castration, of estrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate. PubMed carries no abstract for the reprint, so no patient numbers or values are recorded. The Nobel Foundation summary states that around 1940 Huggins showed that castration, or added female sex hormone, counteracted the disease.

Chemotherapy

  1. 1966 · Understanding · Understanding⚑ needs reviewGleason grading (1966) and ISUP Grade Groups (2014)In 1966 a pathologist, Dr Gleason, published a classification of prostate cancer by the growth patterns of its glands. A 2025 review describes five patterns, with the two most common in a tumour added into a score from 2 to 10. In 2014 pathology experts agreed updated pattern rules and five simpler Grade Groups, reported alongside the Gleason score.Gleason's 1966 classification (no PubMed abstract) is described in a 2025 review as five growth patterns from the VACURG studies, with predominant and secondary patterns added to a score of 2 to 10. The 2014 ISUP consensus (65 pathology experts and 17 clinicians, 19 countries) assigned cribriform and glomeruloid glands to pattern 4 and, with 90% consensus, adopted Grade Groups 1 to 5, validated in over 20,000 prostatectomy specimens.

Molecular origins

  1. 1979 · Detection · Detection & preventionPSA: from purified antigen to serum marker and screening testIn 1979 researchers reported purifying a prostate-specific antigen. In 1987 a study reported that blood levels of it rose with prostate cancer stage and fell after surgery. A 1991 study of men aged 50 or older tested it as a screening tool. Whether screening saves lives was tested later in randomised trials.Stamey 1987 (699 patients, 378 with prostatic cancer): PSA elevated in 122 of 127 with newly diagnosed untreated cancer and in 86% of men with benign prostatic hyperplasia; after radical prostatectomy it fell to undetectable levels (half-life 2.2 days). Catalona 1991 (1653 men aged 50 or older): PSA 4.0 micrograms per litre or higher led to rectal examination and ultrasonography; cancer in 22% of biopsied men with PSA 4.0-9.9 and 67% with 10.0 or higher. Neither abstract reports mortality.
  2. 1982 · Treatment · EndocrineLHRH agonists and medical castration (Tolis, 1982)In 1982 a small study of ten men with prostate cancer reported that daily doses of LHRH agonists, given by injection or nasally, lowered average testosterone by 75% by the third week, with clinical improvement in some men. The authors suggested the drugs could become an alternative to surgical castration and estrogen therapy.Tolis et al., PNAS 1982: ten men with prostatic carcinoma (six stage C, four stage D) given LH-RH agonist analogues for 6 weeks to 12 months; mean plasma testosterone fell 75% by week 3, acid phosphatase fell or normalized by month 2, and serum alkaline phosphatase fell 47% by week 10 in all but one patient. Uncontrolled series. HERO (2020, n=930 treated): sustained castration at 48 weeks 96.7% with oral relugolix versus 88.8% with leuprolide.
  3. 1983 · Treatment · SurgeryWalsh: radical prostatectomy preserving sexual function (1983)A 1982 paper addressed impotence after radical prostatectomy, and a 1983 report described a modified operation designed to avoid injuring the nerves that supply the penis. Twelve men assessed two to ten months after surgery all had erections, and five of the six with partners followed for six months or longer were fully potent.Walsh, Lepor and Eggleston (Prostate 1983) modified radical retropubic prostatectomy: the lateral pelvic fascia is incised anterior to the neurovascular bundle and the lateral pedicle divided close to the prostate. Pathology of 16 specimens showed no compromise of surgical margins. Of 12 men assessed 2-10 months after surgery, all had erections and six achieved penetration and orgasm; five of six (83%) with partners followed 6 months or longer were fully potent.
  4. 1997 · Treatment · RadiationRadiotherapy plus androgen suppression (EORTC 22863)Men with locally advanced prostate cancer were randomly assigned radiotherapy alone or radiotherapy plus three years of an androgen-suppressing injection (goserelin). At five years about four in five men given both treatments were alive, compared with about six in ten given radiotherapy alone. Ten-year results pointed the same way.EORTC 22863 (n=415; locally advanced disease): radiotherapy with or without goserelin for 3 years. 1997 analysis (401 evaluable, median follow-up 45 months): 5-year OS 79% (95% CI 72-86) vs 62% (52-72) with radiotherapy alone, P=0.001. 10-year (median follow-up 9.1 years): OS 58.1% vs 39.8% (HR 0.60, 95% CI 0.45-0.80); clinical DFS 47.7% vs 22.7% (HR 0.42); prostate-cancer mortality 10.3% vs 30.4% (HR 0.38).

Targeted therapy

  1. 2002 · Treatment · SurgeryProstatectomy vs watchful waiting or observation (SPCG-4, PIVOT)Two randomised trials compared removing the prostate with waiting. In a Scandinavian trial, men assigned to surgery were less likely to die of prostate cancer, and the difference persisted for nearly three decades. In an American trial of men diagnosed in the early PSA era, surgery did not significantly reduce deaths from any cause or from prostate cancer.SPCG-4 (n=695): prostate-cancer death 8.9% with watchful waiting vs 4.6% with prostatectomy at median 6.2 years (relative hazard 0.50, 95% CI 0.27-0.91); 15-year cumulative incidence 20.7% vs 14.6%; at 29 years relative risk 0.55 (95% CI 0.41-0.74). PIVOT (n=731, median 10.0 years): all-cause mortality 47.0% with prostatectomy vs 49.9% with observation (HR 0.88, 95% CI 0.71-1.08); prostate-cancer or treatment death 5.8% vs 8.4% (HR 0.63, 95% CI 0.36-1.09).
  2. 2004 · Treatment · Chemotherapy⚑ needs reviewDocetaxel for castration-resistant disease (TAX 327, SWOG 9916)In 2004 two trials compared docetaxel-based chemotherapy with mitoxantrone plus prednisone in men whose metastatic prostate cancer no longer responded to hormone therapy. In TAX 327, docetaxel every three weeks gave a median survival of 18.9 months against 16.5 months. The US FDA approved docetaxel with prednisone in May 2004.TAX 327 (n=1006; prednisone with mitoxantrone, 3-weekly or weekly docetaxel): median OS 16.5, 18.9 and 17.4 months; 3-weekly docetaxel versus mitoxantrone HR 0.76 (95% CI 0.62-0.94; P=0.009), weekly HR 0.91 (0.75-1.11). SWOG 9916 (docetaxel plus estramustine versus mitoxantrone plus prednisone): median OS 17.5 versus 15.6 months, HR 0.80 (0.67-0.97), P=0.02. TAX 327 update (867 deaths): 19.2 versus 16.3 months.
  3. 2009 · De-escalation · SurgeryActive surveillance cohort: selective delayed intervention (Klotz)One academic centre followed almost a thousand men with favourable- or intermediate-risk prostate cancer, offering treatment only if the PSA rose quickly or tests showed progression. After fifteen years, more than nine in ten had not died of prostate cancer and just over half had still not needed treatment.Prospective single-arm cohort (n=993; favorable- or intermediate-risk) managed with an initial expectant approach; intervention offered for PSA doubling time under 3 years, Gleason score progression or clinical progression. Median follow-up from first biopsy among survivors 6.4 years; 15 deaths (1.5%) from prostate cancer. Cause-specific survival 98.1% at 10 and 94.3% at 15 years; 75.7%, 63.5% and 55.0% untreated at 5, 10 and 15 years. The 2010 report (450 men) reclassified 30% as higher risk.
  4. 2009 · Detection · Detection & preventionProstate screening trials: ERSPC, PLCO and Goteborg (2009-2010)In 2009 two large trials asked whether PSA screening lowers deaths from prostate cancer. The European trial reported fewer deaths with screening; the US trial found no clear difference, and many men in its comparison group were also tested. A Swedish trial reported fewer deaths in 2010. All three found more cancers diagnosed with screening.ERSPC (core age group 55-69, n=162,243; median 9 years): prostate cancer death rate ratio 0.80 (95% CI 0.65-0.98). PLCO (76,693 men; annual PSA for 6 years; 7-year follow-up): prostate cancer death rate ratio 1.13 (0.75-1.70); control-arm PSA testing 40% in year 1 to 52% in year 6. Goteborg-1 (20,000 men; PSA every 2 years; median 14 years): rate ratio 0.56 (0.39-0.82). Designs, intervals and follow-up differ; not directly comparable.
  5. 2010 · Treatment · ChemotherapyCabazitaxel after docetaxel (TROPIC)TROPIC compared cabazitaxel plus prednisone with mitoxantrone plus prednisone in 755 men whose metastatic castration-resistant prostate cancer had progressed during or after docetaxel. Median survival was 15.1 months with cabazitaxel and 12.7 months with mitoxantrone. The FDA approved cabazitaxel on 17 June 2010.TROPIC: open-label phase 3, n=755, post-docetaxel mCRPC; cabazitaxel 25 mg/m2 versus mitoxantrone 12 mg/m2, each with prednisone. Final OS 15.1 (95% CI 14.1-16.3) versus 12.7 months (11.6-13.7), HR 0.70 (0.59-0.83; P<0.0001); PFS 2.8 versus 1.4 months. Grade 3 or higher neutropenia 82% versus 58%; febrile neutropenia 8% versus 1%. PROSELICA (n=1200): 20 versus 25 mg/m2 met non-inferiority.
  6. 2010 · Treatment · Immunotherapy⚑ needs reviewSipuleucel-T autologous cellular immunotherapy (IMPACT)Sipuleucel-T is an immunotherapy made from a patient's own blood cells. In the IMPACT trial of 512 men with metastatic castration-resistant prostate cancer, median survival was 25.8 months with sipuleucel-T and 21.7 months with placebo. The FDA licensed it in April 2010; the EU authorisation was withdrawn in 2015 at the manufacturer's request.IMPACT: double-blind, placebo-controlled phase 3, n=512 (2:1), metastatic castration-resistant prostate cancer; sipuleucel-T versus placebo, three infusions every 2 weeks. Median OS 25.8 versus 21.7 months, HR 0.78 (95% CI 0.61-0.98; P=0.03; Cox model adjusted for PSA and LDH); 36-month survival 31.7% versus 23.0%; time to objective progression similar. FDA licensure memo 29 April 2010; EU authorisation 6 September 2013, withdrawn 6 May 2015.

Immunotherapy

  1. 2011 · Treatment · EndocrineAbiraterone after docetaxel improves survival (COU-AA-301)Abiraterone, which blocks androgen production, was tested with prednisone in 1,195 men whose metastatic castration-resistant prostate cancer had progressed after docetaxel. At the first analysis, median survival was 14.8 months with abiraterone against 10.9 months with placebo. The FDA approved it on 28 April 2011.COU-AA-301: randomized (2:1), double-blind phase 3, n=1195, post-docetaxel mCRPC; abiraterone acetate 1000 mg plus prednisone versus placebo plus prednisone. Interim OS (median follow-up 12.8 months): 14.8 versus 10.9 months, HR 0.65 (95% CI 0.54-0.77; P<0.001). Final OS before crossover (median follow-up 20.2 months): 15.8 versus 11.2 months, HR 0.74 (0.64-0.86). Radiologic PFS 5.6 versus 3.6 months. Mineralocorticoid-related adverse events were more frequent with abiraterone.
  2. 2012 · Treatment · EndocrineEnzalutamide after docetaxel (AFFIRM)Enzalutamide, which blocks androgen-receptor signaling, was compared with placebo in 1,199 men whose castration-resistant prostate cancer had progressed after chemotherapy. Median survival was 18.4 months with enzalutamide and 13.6 months with placebo. The FDA approved enzalutamide on 31 August 2012.AFFIRM: randomized (2:1), double-blind, placebo-controlled phase 3, n=1199, castration-resistant prostate cancer after chemotherapy; enzalutamide 160 mg daily versus placebo. Stopped at a planned interim analysis (520 deaths): median OS 18.4 versus 13.6 months, HR 0.63 (95% CI 0.53-0.75; P<0.001); radiographic PFS 8.3 versus 2.9 months (HR 0.40). Seizures were reported in five patients (0.6%) given enzalutamide.
  3. 2012 · Detection · Detection & preventionUSPSTF PSA screening recommendations (2012, 2018)In 2008 the US Preventive Services Task Force said the evidence was too thin to judge PSA screening for men under 75. In 2012 it recommended against PSA-based screening for all men in the general US population. In 2018 it changed this to an individual decision for ages 55 to 69, keeping the recommendation against screening from age 70.USPSTF 2008: insufficient evidence for men younger than 75 (I statement), against screening at 75 and older (grade D). 2012: against PSA-based screening for men in the general US population regardless of age (grade D). 2018: grade C for ages 55-69 (individual decision), grade D from 70. The 2018 statement estimates that screening men aged 55-69 may prevent about 1.3 prostate cancer deaths over about 13 years and about 3 metastatic cases per 1000 men screened.
  4. 2013 · Treatment · Radiation⚑ needs reviewRadium-223 and survival in bone-metastatic CRPC (ALSYMPCA)Radium-223 is a radioactive drug that gives off alpha particles and targets bone metastases. In ALSYMPCA, men with castration-resistant prostate cancer and bone metastases who received it lived longer than those given placebo: about 15 months versus 11 months in the updated analysis, with low rates of bone-marrow suppression.Phase 3, double-blind trial (N=921) in castration-resistant prostate cancer with bone metastases: radium-223 (50 kBq/kg, six 4-weekly injections) versus placebo, 2:1, plus best standard of care. Primary endpoint OS. Interim analysis (809 patients): median 14.0 vs 11.2 months, HR 0.70 (95% CI 0.55-0.88; P=0.002). Updated analysis (528 deaths, before crossover): 14.9 vs 11.3 months, HR 0.70 (0.58-0.83; P<0.001).
  5. 2015 · Treatment · ChemotherapyDocetaxel with ADT in hormone-sensitive disease (CHAARTED, STAMPEDE)In 2015 two large trials, CHAARTED and STAMPEDE, reported longer survival when docetaxel chemotherapy was started together with hormone therapy. In CHAARTED, median survival was 57.6 months with docetaxel and 44.0 months without. A smaller French trial, GETUG-AFU 15, had found no significant survival difference.CHAARTED (n=790; metastatic hormone-sensitive; ADT with or without docetaxel x6): median OS 57.6 versus 44.0 months, HR 0.61 (95% CI 0.47-0.80; P<0.001). STAMPEDE (n=2962 randomized across four arms; 61% M+): docetaxel plus standard of care versus standard of care HR 0.78 (0.66-0.93; P=0.006); zoledronic acid HR 0.94 (0.79-1.11). GETUG-AFU 15 (n=385): median OS 58.9 versus 54.2 months, HR 1.01 (0.75-1.36). STAMPEDE and GETUG-AFU 15 were open-label.
  6. 2016 · De-escalation · RadiationShorter radiotherapy: hypofractionation and SBRT (CHHiP, PACE-B)Several randomised trials tested giving prostate radiotherapy in fewer, larger doses. In the largest, twenty treatments over four weeks was shown not to be worse for cancer control than thirty-seven over seven weeks, with similar long-term side-effects. Later trials tested seven or five treatments; for five-treatment stereotactic radiotherapy only two-year side-effect results are included here.CHHiP (n=3216): 5-year BCF-free survival 88.3% (74 Gy/37 fractions), 90.6% (60 Gy/20) and 85.9% (57 Gy/19); 60 Gy non-inferior (HR 0.84, 90% CI 0.68-1.03), 57 Gy not shown non-inferior (HR 1.20). PROFIT (60 Gy/20 vs 78 Gy/39): 85% in both arms. HYPO-RT-PC: 84% in both arms. PACE-B at 24 months, grade 2+ genitourinary toxicity 2% (conventional) vs 3% (SBRT); gastrointestinal 3% vs 2%.
  7. 2016 · Understanding · Understanding⚑ needs reviewGermline DNA-repair gene variants in metastatic prostate cancerTesting blood DNA from 692 men with metastatic prostate cancer found harmful inherited changes in DNA-repair genes in about 12 in 100 men (11.8%), compared with about 5 in 100 men with localised cancer (4.6%). BRCA2 was the most frequent gene. Family history and age at diagnosis did not distinguish carriers.Multicentre sequencing of germline DNA from 692 men with metastatic prostate cancer, unselected for family history or age, in 20 DNA-repair genes: 84 presumed-deleterious mutations in 82 men (11.8%), including BRCA2 5.3% (37 men), ATM 1.6%, CHEK2 1.9% (of 534 men with data) and BRCA1 0.9%. Localised disease: 4.6% (499 men); ExAC: 2.7% (53,105 people); both P<0.001. No difference by family history or age.
  8. 2016 · Treatment · SurgeryProtecT: monitoring, surgery or radiotherapy for PSA-detected cancerA UK trial assigned about sixteen hundred men whose prostate cancer was found by PSA testing to monitoring, surgery or radiotherapy. After fifteen years, around three in a hundred men or fewer in each group had died of prostate cancer. Roughly half as many men developed metastases after surgery or radiotherapy as after monitoring, with different side-effects.ProtecT (n=1643, aged 50-69, PSA-detected localized disease) randomised men to active monitoring (545), prostatectomy (553) or radiotherapy (545). At median 15 years, prostate-cancer death occurred in 3.1%, 2.2% and 2.9% (P=0.53); metastases in 9.4%, 4.7% and 5.0%; clinical progression in 25.9%, 10.5% and 11.0%. Patient-reported erections sufficient for intercourse at 7 years: 18% (surgery), 30% (monitoring), 27% (radiotherapy).
  9. 2017 · Treatment · EndocrineAbiraterone with ADT in hormone-sensitive disease (LATITUDE, STAMPEDE)In 2017 two trials added abiraterone, which blocks androgen production, to hormone therapy at the start of treatment for metastatic prostate cancer. In LATITUDE, median survival at the final analysis was 53.3 months with abiraterone and 36.5 months with placebo. The FDA approved this use for high-risk disease in February 2018.LATITUDE (n=1199; high-risk metastatic castration-sensitive; ADT plus abiraterone and prednisone versus ADT plus placebos): interim OS HR 0.62 (95% CI 0.51-0.76), rPFS 33.0 versus 14.8 months (HR 0.47); final OS 53.3 versus 36.5 months, HR 0.66 (0.56-0.78), with crossover allowed after the interim analysis. STAMPEDE abiraterone comparison (n=1917; 52% metastatic): OS HR 0.63 (0.52-0.76); failure-free survival HR 0.29 (0.25-0.34). Hypertension and hypokalemia were more frequent with abiraterone.
  10. 2017 · Detection · Detection & prevention⚑ needs reviewMRI before biopsy: PROMIS and PRECISIONTwo studies tested MRI before a prostate biopsy. In PROMIS, MRI detected more clinically significant cancers than a standard ultrasound-guided biopsy but ruled fewer men out correctly. In the randomised PRECISION trial, MRI first, with a targeted biopsy only if suspicious, found more significant cancers and fewer insignificant ones than standard biopsy.PROMIS (576 men with PSA up to 15 ng/mL, no prior biopsy; reference template mapping biopsy): sensitivity for clinically significant cancer 93% (95% CI 88-96) for MRI vs 48% (42-55) for TRUS biopsy; specificity 41% vs 96%. PRECISION (500 randomised): clinically significant cancer 38% with MRI-targeted biopsy vs 26% with standard biopsy (adjusted difference 12 percentage points, 95% CI 4-20; P=0.005); 28% avoided biopsy. STHLM3-MRI and Goteborg-2 extend this to screening.
  11. 2018 · Treatment · EndocrineAR inhibitors and metastasis-free survival in non-metastatic CRPCThree trials, SPARTAN, PROSPER and ARAMIS, tested androgen-receptor inhibitors in men with non-metastatic castration-resistant prostate cancer and a rapidly rising PSA. Each reported longer metastasis-free survival than placebo, for example 40.5 months with apalutamide against 16.2 months. Later reports of overall survival also favored each drug.Non-metastatic CRPC on conventional imaging, PSA doubling time 10 months or less, placebo-controlled (2:1) with continued ADT. Metastasis-free survival: SPARTAN (n=1207) 40.5 versus 16.2 months, HR 0.28 (95% CI 0.23-0.35); PROSPER (n=1401) 36.6 versus 14.7 months, HR 0.29 (0.24-0.35); ARAMIS (n=1509) 40.4 versus 18.4 months, HR 0.41 (0.34-0.50). Final overall survival HRs: SPARTAN 0.78 (0.64-0.96), PROSPER 0.73 (0.61-0.89), ARAMIS 0.69 (0.53-0.88).
  12. 2019 · Treatment · EndocrineAR inhibitors with ADT, hormone-sensitive (TITAN, ARCHES, ENZAMET)In 2019 three trials, TITAN, ARCHES and ENZAMET, added an androgen-receptor inhibitor to hormone therapy for metastatic hormone-sensitive prostate cancer, each against its own control. All three reported longer survival without progression or longer overall survival. In TITAN, 82.4% of men on apalutamide were alive at two years, against 73.5% on placebo.TITAN (n=1052; apalutamide versus placebo, plus ADT): 24-month rPFS 68.2% versus 47.5% (HR 0.48; 95% CI 0.39-0.60), interim OS HR 0.67 (0.51-0.89), final OS HR 0.65 (0.53-0.79). ARCHES (n=1150; enzalutamide versus placebo): rPFS HR 0.39 (0.30-0.50); final OS HR 0.66 (0.53-0.81). ENZAMET (n=1125; open-label; control a standard antiandrogen): OS HR 0.67 (0.52-0.86); planned analysis HR 0.70 (0.58-0.84).

Precision & engineered

  1. 2020 · Treatment · Targeted⚑ needs reviewPARP inhibitors for HRR-altered mCRPC (PROfound, TRITON)Some prostate cancers carry changes in DNA-repair genes such as BRCA2. After a hormonal drug stopped working, olaparib (PROfound) and rucaparib (TRITON3) delayed progression compared with the control drugs in men whose tumours had those changes: about 7 versus 4 months with olaparib. Olaparib also lengthened survival in the BRCA1, BRCA2 and ATM group.PROfound (phase 3, N=387; progression on enzalutamide or abiraterone, HRR alteration): cohort A (BRCA1, BRCA2 or ATM) imaging-based PFS 7.4 vs 3.6 months (HR 0.34; 95% CI 0.25-0.47); final OS 19.1 vs 14.7 months (HR 0.69; 0.50-0.97), 66% of controls crossing over. TRITON3 (phase 3, N=405): BRCA subgroup rPFS 11.2 vs 6.4 months (HR 0.50; 0.36-0.69). TRITON2 (phase 2): BRCA ORR 43.5% by independent review.
  2. 2020 · Detection · UnderstandingPSMA PET-CT before curative-intent treatment (proPSMA)A 2020 Australian randomised study compared two ways of staging men with high-risk prostate cancer before surgery or radiotherapy: CT with a bone scan, or PSMA PET-CT. PSMA PET-CT was more accurate at finding spread to pelvic lymph nodes or distant sites, and management changed more often. The report gives imaging accuracy, not survival.proPSMA (302 randomised, ten Australian hospitals, high-risk localised disease): accuracy for pelvic nodal or distant metastasis 92% (95% CI 88-95) with gallium-68 PSMA-11 PET-CT vs 65% (60-69) with CT plus bone scan (difference 27%, 95% CI 23-31; p<0.0001). Sensitivity 85% vs 38%; specificity 98% vs 91%. First-line imaging changed management in 28% (PSMA PET-CT) vs 15% (conventional) (p=0.008). Primary endpoint was accuracy; no survival data.
  3. 2021 · Treatment · Radiation⚑ needs review177Lu-PSMA-617 for PSMA-positive mCRPC (VISION, TheraP)A radioactive drug that attaches to PSMA, a protein highly expressed in metastatic castration-resistant prostate cancer, was tested after standard drugs stopped working. In VISION, adding it to standard care delayed progression (about 9 versus 3 months) and extended survival (about 15 versus 11 months). In TheraP, survival did not differ from cabazitaxel, with fewer severe side effects.VISION (phase 3, N=831; PSMA-PET-positive mCRPC after an ARPI and one or two taxanes): 177Lu-PSMA-617 plus standard care vs standard care alone. Imaging-based PFS 8.7 vs 3.4 months (HR 0.40; 99.2% CI 0.29-0.57); OS 15.3 vs 11.3 months (HR 0.62; 95% CI 0.52-0.74). TheraP (phase 2, N=200, vs cabazitaxel): PSA response 66% vs 37%; OS RMST 19.1 vs 19.6 months (P=0.77).
  4. 2022 · Treatment · EndocrineTriplet therapy: ADT, docetaxel and an AR inhibitor (ARASENS, PEACE-1)In 2022 two trials added a third drug to hormone therapy plus docetaxel in metastatic hormone-sensitive prostate cancer. In ARASENS, adding darolutamide gave a hazard ratio for death of 0.68 against placebo. In PEACE-1, adding abiraterone gave 0.75 among men who received docetaxel. The FDA approved darolutamide with docetaxel in August 2022.ARASENS (n=1306; darolutamide 600 mg twice daily versus placebo, both with ADT and docetaxel): OS HR 0.68 (95% CI 0.57-0.80; P<0.001). PEACE-1 (open-label 2x2 factorial; de novo metastatic castration-sensitive): abiraterone versus none in the ADT-plus-docetaxel population (355 per group), OS HR 0.75 (95.1% CI 0.59-0.95; P=0.017), rPFS HR 0.50 (99.9% CI 0.34-0.71). Grade 3 or worse adverse events in that population: 63% versus 52%.
  5. 2022 · Treatment · TargetedPARP inhibitor plus ARPI first line (PROpel, MAGNITUDE, TALAPRO-2)Three large trials added a PARP inhibitor to a hormonal drug as first treatment for metastatic castration-resistant prostate cancer. Each delayed progression on imaging; in MAGNITUDE and TALAPRO-2 the effect looked larger with BRCA or other DNA-repair gene changes. Final survival was longer with talazoparib plus enzalutamide (about 46 versus 37 months) but not significantly different in PROpel or MAGNITUDE.First-line mCRPC, PARP inhibitor plus ARPI vs placebo plus ARPI. PROpel (olaparib + abiraterone, all-comers): imaging-based PFS 24.8 vs 16.6 months (HR 0.66); final OS 42.1 vs 34.7 months (HR 0.81; 95% CI 0.67-1.00; P=0.054). MAGNITUDE (niraparib + abiraterone, HRR+): rPFS HR 0.73; final OS HR 0.931 (0.720-1.203). TALAPRO-2 (talazoparib + enzalutamide): rPFS HR 0.63; final OS 45.8 vs 37.0 months (HR 0.80; 0.66-0.96).
  6. 2023 · Treatment · EndocrineEnzalutamide for high-risk biochemical recurrence (EMBARK)EMBARK tested enzalutamide in 1,068 men whose prostate cancer had a rising PSA, called biochemical recurrence, with a high risk of progression. At five years, 87.3% of men on enzalutamide plus leuprolide were free of metastasis and alive, against 71.4% on leuprolide alone. The FDA approved this use on 16 November 2023.EMBARK (n=1068; phase 3): high-risk biochemical recurrence, PSA doubling time 9 months or less. Enzalutamide plus leuprolide, placebo plus leuprolide, or enzalutamide alone. Primary end point MFS (blinded independent central review); median follow-up 60.7 months. 5-year MFS 87.3% versus 71.4%, HR 0.42 (95% CI 0.30-0.61; P<0.001); enzalutamide alone 80.0%, HR 0.63 (0.46-0.87; P=0.005). The abstract reports no overall survival.
  7. 2024 · Treatment · EndocrineDarolutamide plus ADT without docetaxel (ARANOTE)ARANOTE tested darolutamide added to hormone therapy, without chemotherapy, in 669 men with metastatic hormone-sensitive prostate cancer. The hazard ratio for radiological progression or death was 0.54 against placebo plus hormone therapy. Overall survival results at that point were described as suggestive of benefit. The FDA approved this use on 3 June 2025.ARANOTE (phase 3, 2:1, n=669): darolutamide 600 mg twice daily or placebo with ADT, without docetaxel. At the primary cutoff (7 June 2024): rPFS HR 0.54 (95% CI 0.41-0.71; P<0.0001) with consistent benefit in high- and low-volume disease; OS HR 0.81 (0.59-1.12); time to metastatic castration-resistant disease HR 0.40 (0.32-0.51). Discontinuation for adverse events 6.1% versus 9.0%.
  8. 2024 · Detection · Detection & preventionScreening follow-up: CAP (15-year) and ERSPC (23-year)Longer follow-up of the European screening trial, now 23 years, still showed fewer prostate cancer deaths in the screening group, alongside more cancers diagnosed. A UK trial offering a single PSA test found no clear difference at 10 years and a small reduction in deaths at 15 years. In both, the absolute difference was well under one percentage point.ERSPC core age group (n=162,236; median 23 years): prostate cancer mortality rate ratio 0.87 (95% CI 0.80-0.95), absolute risk reduction 0.22%; 456 men invited and 12 diagnosed per death averted. CAP (single PSA invitation, men aged 50-69, primary care practices): rate ratio 0.96 (0.85-1.08) at 10 years; 0.92 (0.85-0.99) at 15 years, cumulative risk of prostate cancer death 0.69% vs 0.78%; all-cause mortality rate ratio 0.97 (0.94-1.01).
  9. 2024 · Treatment · Radiation⚑ needs review177Lu-PSMA-617 before taxane chemotherapy (PSMAfore)In men with PSMA-positive metastatic castration-resistant prostate cancer who had progressed on one hormonal drug and not yet had chemotherapy, a PSMA-targeted radioactive drug delayed progression on imaging more than switching hormonal drugs: about 12 versus 6 months. Final survival did not differ, and 60% of the comparison group crossed over to the radioligand.PSMAfore (phase 3, open-label, N=468): taxane-naive, PSMA-positive mCRPC progressing on one ARPI; 177Lu-PSMA-617 vs change of ARPI. rPFS median 9.30 vs 5.55 months (HR 0.41; 95% CI 0.29-0.56); updated 11.60 vs 5.59 months (HR 0.49; 0.39-0.61). Final OS 24.48 vs 23.13 months (ITT HR 0.91; 0.72-1.14; P=0.20), with 60.3% of the control arm crossing over.
  10. 2025 · Treatment · Targeted⚑ needs reviewBiomarker-selected mHSPC: AMPLITUDE (BRCA) and CAPItello-281 (PTEN)Two phase 3 trials added a targeted drug to abiraterone from the start of hormone therapy in men whose cancer had spread but was still hormone-sensitive and carried a specific tumour change: DNA-repair gene alterations (niraparib) or PTEN loss (capivasertib). Both delayed progression on imaging; survival data were immature. FDA approvals are narrower: BRCA2 mutations and PTEN-deficient tumours.AMPLITUDE (phase 3, N=696, HRR-altered mCSPC): niraparib + abiraterone/prednisone vs placebo + same; rPFS HR 0.52 in the BRCA subgroup (95% CI 0.37-0.72) and 0.63 overall (0.49-0.80); OS immature (HR 0.79; 0.59-1.04). CAPItello-281 (phase 3, PTEN-deficient mHSPC, N=1012): capivasertib + abiraterone, rPFS 33.2 vs 25.7 months (HR 0.81; 0.66-0.98); OS HR 0.90 (0.71-1.15; 26.4% maturity).
  11. 2026 · Treatment · Radiation⚑ needs review177Lu-PSMA-617 plus ARPI in PSMA-positive mHSPC (PSMAddition)In men with PSMA-positive prostate cancer that had spread but was still hormone-sensitive, adding a PSMA-targeted radioactive drug to standard hormone treatment lowered the risk of progression on imaging or death by 28% at the second interim analysis. Survival data were immature. The FDA approved this use on 31 July 2026, before the results were published.PSMAddition (phase 3, open-label, N=1144): PSMA-positive metastatic hormone-sensitive disease, 177Lu-PSMA-617 plus ADT and ARPI vs ADT plus ARPI. Second interim analysis (data cutoff 13 January 2025): rPFS by blinded central assessment HR 0.72 (95% CI 0.58-0.90; P=0.0021), median not reached in either arm; 139 (24%) vs 172 (30%) events. Overall survival immature per the FDA.

Then and now

  • 5-year relative survival · United States, SEER 8 registries

    • 67.68%

      1975 (observed value; first year in the table)

    Males, all races (the table note reads 'All Races, Males'); prostate cancer, all stages combined; the page states no age range for this series.

    Observed single-year value; the adjacent modelled-trend value for 1975 is 67.81%. SEER 8 five-year relative survival table on the SEER Cancer Stat Facts prostate page. The table column is headed 'Year' and the chart footnote reads 'SEER 8 5-Year Relative Survival Percent from 1975-2018, All Races, Males'; neither labels the year as year of diagnosis. Relative survival excludes the risk of dying from other causes. Changes in detection can alter stage mix, lead time and overdiagnosis (the incidence column in the same table rises from 117.29 per 100,000 in 1986 to 224.93 in 1992 and then falls), so a change in this series can reflect treatment, earlier and more frequent diagnosis, or both; the page attributes none of the change to any cause. Compare only with other values from the same SEER 8 series.

    Source

  • 5-year relative survival · United States, SEER 8 registries

    • 89.71%

      1990 (observed value)

    Males, all races (the table note reads 'All Races, Males'); prostate cancer, all stages combined; the page states no age range for this series.

    Observed single-year value; modelled trend for 1990 is 91.03%. Shown because the series had already risen steeply by 1990: the modelled trend is 77.74% in 1986 and 95.13% in 1992, the same years in which the incidence column rises from 117.29 to 224.93 per 100,000. SEER 8 five-year relative survival table on the SEER Cancer Stat Facts prostate page. The table column is headed 'Year' and the chart footnote reads 'SEER 8 5-Year Relative Survival Percent from 1975-2018, All Races, Males'; neither labels the year as year of diagnosis. Relative survival excludes the risk of dying from other causes. Changes in detection can alter stage mix, lead time and overdiagnosis (the incidence column in the same table rises from 117.29 per 100,000 in 1986 to 224.93 in 1992 and then falls), so a change in this series can reflect treatment, earlier and more frequent diagnosis, or both; the page attributes none of the change to any cause. Compare only with other values from the same SEER 8 series.

    Source

  • 5-year relative survival · United States, SEER 8 registries

    • 95.71%

      1995 (observed value)

    Males, all races (the table note reads 'All Races, Males'); prostate cancer, all stages combined; the page states no age range for this series.

    Observed single-year value; modelled trend for 1995 is 95.29%. From 1996 to 2018 the observed series stays between 96.82% (1996) and 100.00% (2001), with 97.27% in 2015; the largest rise in the observed series is between 1986 (77.95%) and 1995. SEER 8 five-year relative survival table on the SEER Cancer Stat Facts prostate page. The table column is headed 'Year' and the chart footnote reads 'SEER 8 5-Year Relative Survival Percent from 1975-2018, All Races, Males'; neither labels the year as year of diagnosis. Relative survival excludes the risk of dying from other causes. Changes in detection can alter stage mix, lead time and overdiagnosis (the incidence column in the same table rises from 117.29 per 100,000 in 1986 to 224.93 in 1992 and then falls), so a change in this series can reflect treatment, earlier and more frequent diagnosis, or both; the page attributes none of the change to any cause. Compare only with other values from the same SEER 8 series.

    Source

  • 5-year relative survival · United States, SEER 8 registries

    • 98.65%

      2018 (observed value; last observed year in the table)

    Males, all races (the table note reads 'All Races, Males'); prostate cancer, all stages combined; the page states no age range for this series.

    Observed single-year value; modelled trend for 2018 is 98.48%. Observed values for 2019 to 2023 appear as '-' in the table (the page gives no reason) while the modelled-trend column continues to 99.30% for 2023. SEER 8 five-year relative survival table on the SEER Cancer Stat Facts prostate page. The table column is headed 'Year' and the chart footnote reads 'SEER 8 5-Year Relative Survival Percent from 1975-2018, All Races, Males'; neither labels the year as year of diagnosis. Relative survival excludes the risk of dying from other causes. Changes in detection can alter stage mix, lead time and overdiagnosis (the incidence column in the same table rises from 117.29 per 100,000 in 1986 to 224.93 in 1992 and then falls), so a change in this series can reflect treatment, earlier and more frequent diagnosis, or both; the page attributes none of the change to any cause. Compare only with other values from the same SEER 8 series.

    Source

  • 5-year relative survival · United States, SEER 21 registries (excluding IL)

    • 98.2%

      2016-2022 (as labelled on the page)

    Prostate cancer, all stages combined; the page headline gives no sex or race (the stage table on the same page is labelled 'All Races, Males').

    Different registry grouping from the SEER 8 series and a multi-year figure, so it is not comparable with the 1975 value and should not be subtracted from SEER 8 values. By SEER Combined Summary Stage on the same page: localized 100.0% (69% of cases), regional 100.0% (14%), distant 40.1% (9%), unknown stage 94.1% (8%); percentages of cases are rounded as shown. Relative survival is a registry estimate that excludes other-cause mortality and, in a screened population can include cancers found through screening that might not otherwise have been diagnosed (overdiagnosis is discussed on the USPSTF recommendation page, not on the SEER page); the page notes that such statistics cannot predict what will happen to an individual.

    Source

  • 5-year relative survival · United States, SEER 21 registries (excluding IL)

    • 40.1%

      2016-2022, distant stage at diagnosis

    Males, all races, distant stage (cancer has metastasized) by SEER Combined Summary Stage; about 9% of cases in this series are distant stage at diagnosis.

    Stage-specific figure from the same SEER 21 table as the 98.2% all-stage value; do not compare with the SEER 8 series. Registry stage categories are not the same as the imaging-defined metastatic disease used in trials.

    Source

  • Age-standardised mortality · United States (national mortality)

    • 30.94per 100,000

      1975 (observed value; first year in the table)

    Males, all races; age-adjusted rate.

    The adjacent modelled-trend value for 1975 is 31.39. US mortality (National Center for Health Statistics), not SEER registry data; the page states that deaths come from U.S. Mortality. Single-year observed value. Mortality is shown beside survival because survival can rise through earlier diagnosis and case-mix change as well as treatment; the page does not separate these, and the effect of PSA screening on prostate cancer mortality is a separate evidence question.

    Source

  • Age-standardised mortality · United States (national mortality)

    • 39.88per 100,000

      1993 (highest observed value in the table)

    Males, all races; age-adjusted rate.

    Modelled trend for 1993 is 39.59. The neighbouring observed values are 39.74 (1992) and 39.04 (1994). US mortality (National Center for Health Statistics), not SEER registry data. Single-year observed value, shown as the peak of the observed series on the page; the page makes no causal statement about the peak or the later fall.

    Source

  • Age-standardised mortality · United States (national mortality)

    • 18.4per 100,000

      2024 (observed value; last year in the table)

    Males, all races; age-adjusted rate.

    Modelled trend for 2024 is 18.42; the 2020-2024 pooled rate given in the page text is 18.9 per 100,000 men per year, and the page reports death rates falling on average 0.8% each year over 2015-2024. Rates differ by group on the same page for 2020-2024: 36.2 for non-Hispanic Black men and 18.1 for non-Hispanic White men. US mortality (National Center for Health Statistics), not SEER registry data. Single-year observed value.

    Source

  • 10-year relative survival · United Kingdom

    • 21.7%

      Diagnosed in the 1970s

    Males diagnosed with prostate cancer in the UK (the page's wording); no age range stated for this figure.

    Cancer Research UK words this as 'more than 1 in 5 (21.7%)' of males diagnosed in the 1970s having 'survived their disease beyond ten years'. The page does not say whether the figure is net or relative survival, which UK nations are included for the 1970s, or the exact years. The page states that survival trends reflect a combination of changes in treatment and stage distribution; the page does not mention testing practice. Different source, country and measure from the SEER series; do not compare directly with them.

    Source

  • 10-year relative survival · United Kingdom

    • 78.9%

      2018 (the page says 'predicted')

    Males diagnosed with prostate cancer in the UK; the page also gives 94.2% for ages 15-44 and 67.5% for ages 75-99 (UK, 2018).

    The page states that 'around 8 in 10 (78.9%)' males diagnosed with prostate cancer in the UK are predicted to survive their disease for ten years or more (2018); this is a predicted figure, not observed ten-year follow-up of that year's cases, and the page does not describe the prediction method or whether it is net or relative survival. The page also states that five-year relative survival is below the European average in England, Wales and Scotland and similar to it in Northern Ireland. Different source, country and measure from the SEER series.

    Source

Survival figures are affected by earlier detection (lead time) and overdiagnosis, and by changes in who is diagnosed. For screened cancers, read them alongside mortality.

Evidence chains

A lane follows one defined population and setting, where each new trial tests against what was then standard. Compare only within a lane, and read every comparison as illustrative.

Metastatic hormone-sensitive, add-on to ADT: overall survival

Men starting androgen deprivation therapy (ADT) for metastatic hormone-sensitive (castration-sensitive) prostate cancer · Metastatic · endpoint: OS

Results are not comparable across trials.

Eras, eligibility and control arms differ. CHAARTED and GETUG-AFU 15 added docetaxel to ADT; LATITUDE enrolled only newly diagnosed high-risk disease and, after its first interim analysis, allowed placebo patients to cross over; the STAMPEDE figure is the metastatic-only comparison from its 2023 report, in which the control group could receive docetaxel from December 2015. ENZAMET compared enzalutamide with a standard antiandrogen and reports 5-year survival percentages, so it is listed but not drawn on the median axis. TITAN, ARCHES, ARASENS, PEACE-1 and ARANOTE are listed without arm medians (hazard ratios or one arm only) and are not drawn; in ARASENS the control arm also received docetaxel. Compare only each trial's own two arms.

Each pair shows one trial: its control arm and its experimental arm. Yesterday's experimental arm is often today's control. Populations, definitions and follow-up differ.

020406080OS, median (months)2015201520172017CHAARTEDGETUG-AFU 15LATITUDESTAMPEDE
  • experimental arm
  • control arm
  • different endpoint from the lane's
  • step line through experimental values
OS, median, across 4 trials in this lane. CHAARTED (2015): experimental 57.6 months vs control 44 months; GETUG-AFU 15 (2015): experimental 58.9 months vs control 54.2 months; LATITUDE (2017): experimental 53.3 months vs control 36.5 months; STAMPEDE (2017): experimental 76.6 months vs control 45.7 months.
Data table
TrialYearEndpointControl (months)Experimental (months)
CHAARTED2015OS44 months57.6 months
GETUG-AFU 152015OS54.2 months58.9 months
LATITUDE2017OS36.5 months53.3 months
STAMPEDE2017OS45.7 months76.6 months
ENZAMET2019OS (not plotted: different measure or time point)57 %67 %

Metastatic castration-resistant, after docetaxel: overall survival

Men with metastatic castration-resistant prostate cancer that progressed during or after docetaxel-based chemotherapy · Metastatic · endpoint: OS

Results are not comparable across trials.

The three trials enrolled men after chemotherapy but compared against different controls: mitoxantrone plus prednisone in TROPIC and placebo (with prednisone in COU-AA-301) in the other two. AFFIRM's figure is from a planned interim analysis and its population is described as men after chemotherapy; COU-AA-301's is its final analysis before crossover. Prior-therapy rules, performance status and follow-up differ, and no trial here compares these drugs with each other. CARD and PROSELICA, which are in the cabazitaxel milestone, are a different population and design and are not drawn. Compare only each trial's own two arms.

Each pair shows one trial: its control arm and its experimental arm. Yesterday's experimental arm is often today's control. Populations, definitions and follow-up differ.

0510152025OS, median (months)201020112012TROPICCOU-AA-301AFFIRM
  • experimental arm
  • control arm
  • different endpoint from the lane's
  • step line through experimental values
OS, median, across 3 trials in this lane. TROPIC (2010): experimental 15.1 months vs control 12.7 months; COU-AA-301 (2011): experimental 15.8 months vs control 11.2 months; AFFIRM (2012): experimental 18.4 months vs control 13.6 months.
Data table
TrialYearEndpointControl (months)Experimental (months)
TROPIC2010OS12.7 months15.1 months
COU-AA-3012011OS11.2 months15.8 months
AFFIRM2012OS13.6 months18.4 months

Localized disease: prostate cancer mortality with surgery, radiotherapy or monitoring

Men with clinically localized prostate cancer randomized to treatment or to watchful waiting, observation or active monitoring · Localised · endpoint: Prostate cancer mortality

Results are not comparable across trials.

These results are not like for like. SPCG-4 reports cumulative incidence at 15 years; PIVOT (men detected in the early PSA era) reports a proportion of men followed up to 19.5 years (median 12.7); ProtecT (PSA-detected disease, active monitoring as the reference arm) reports a proportion at a median of 15 years. Only SPCG-4 is drawn. ProtecT and PIVOT are listed with their own values but not plotted beside it, because the measures and follow-up differ. Comparators also differ (watchful waiting, observation, active monitoring), and ProtecT's third arm, radiotherapy, is not shown. Compare only each trial's own arms.

Each pair shows one trial: its control arm and its experimental arm. Yesterday's experimental arm is often today's control. Populations, definitions and follow-up differ.

020406080100Prostate cancer mortality at 180 months (%)2002SPCG-4
  • experimental arm
  • control arm
  • different endpoint from the lane's
  • step line through experimental values
Prostate cancer mortality at 180 months, rate, across 1 trial in this lane. SPCG-4 (2002): experimental 14.6 % vs control 20.7 %.
Data table
TrialYearEndpointControl (%)Experimental (%)
SPCG-42002Prostate cancer mortality20.7 %14.6 %
PIVOT2002Prostate cancer mortality (not plotted: different measure or time point)11.4 %7.4 %
ProtecT2016Prostate cancer mortality (not plotted: different measure or time point)3.1 %2.2 %

PSA screening: prostate cancer mortality

Men invited to PSA screening versus men not invited, in population-based randomized trials · Screening · endpoint: Prostate cancer mortality

Results are not comparable across trials.

The two trials with arm values use different designs and measures and are not placed on one axis. Goteborg-1 invited men to repeat PSA testing every 2 years and reports cumulative risk of death from prostate cancer at 14 years; CAP offered a single PSA test and reports cumulative percentages at a median of 15 years. Age ranges, PSA thresholds and biopsy practice differ. ERSPC and PLCO report rate ratios rather than arm values and are listed in the milestones, not drawn; Goteborg-1 overlaps ERSPC. Absolute differences are small and must be read beside the overdiagnosis figures in the milestones. Compare only each trial's own two arms.

Each pair shows one trial: its control arm and its experimental arm. Yesterday's experimental arm is often today's control. Populations, definitions and follow-up differ.

020406080100Prostate cancer mortality at 168 months (%)2009Göteborg-1
  • experimental arm
  • control arm
  • different endpoint from the lane's
  • step line through experimental values
Prostate cancer mortality at 168 months, rate, across 1 trial in this lane. Göteborg-1 (2009): experimental 0.5 % vs control 0.9 %.
Data table
TrialYearEndpointControl (%)Experimental (%)
Göteborg-12009Prostate cancer mortality0.9 %0.5 %
CAP2024Prostate cancer mortality (not plotted: different measure or time point)0.78 %0.69 %

PARP inhibitors after an androgen-receptor drug: BRCA1, BRCA2 or ATM alterations

Metastatic castration-resistant prostate cancer with a BRCA1, BRCA2 or ATM alteration and progression after enzalutamide or abiraterone · Metastatic · endpoint: rPFS

Results are not comparable across trials.

PROfound cohort A (olaparib) and the TRITON3 intention-to-treat population (rucaparib) both enrolled men with BRCA1, BRCA2 or ATM alterations after progression on a new hormonal agent. PROfound's control was enzalutamide or abiraterone; TRITON3's physician's-choice control also included docetaxel. Review methods, crossover handling and follow-up are as published in each paper and differ. First-line combination trials enrolled a different population and are shown in separate lanes. Compare only each trial's own two arms.

Each pair shows one trial: its control arm and its experimental arm. Yesterday's experimental arm is often today's control. Populations, definitions and follow-up differ.

02468101214rPFS, median (months)20202020PROfoundTRITON3
  • experimental arm
  • control arm
  • different endpoint from the lane's
  • step line through experimental values
rPFS, median, across 2 trials in this lane. PROfound (2020): experimental 7.4 months vs control 3.6 months; TRITON3 (2020): experimental 10.2 months vs control 6.4 months.
Data table
TrialYearEndpointControl (months)Experimental (months)
PROfound2020rPFS3.6 months7.4 months
TRITON32020rPFS6.4 months10.2 months

First-line PARP inhibitor plus androgen-receptor drug: not selected for DNA-repair alterations

First-line metastatic castration-resistant prostate cancer, enrolled regardless of homologous recombination repair (HRR) gene status · Metastatic · endpoint: rPFS

Results are not comparable across trials.

PROpel added olaparib to abiraterone and reports the planned primary analysis, with progression assessed by the investigator. TALAPRO-2 added talazoparib to enzalutamide; its median here is from an updated descriptive analysis, because the talazoparib median was not reached at the primary analysis, and its primary endpoint used blinded central review. The backbone drug, follow-up and review method differ. MAGNITUDE, which analysed the HRR-positive cohort first, is in the next lane. Compare only each trial's own two arms.

Each pair shows one trial: its control arm and its experimental arm. Yesterday's experimental arm is often today's control. Populations, definitions and follow-up differ.

010203040rPFS, median (months)20222022PROpelTALAPRO-2
  • experimental arm
  • control arm
  • different endpoint from the lane's
  • step line through experimental values
rPFS, median, across 2 trials in this lane. PROpel (2022): experimental 24.8 months vs control 16.6 months; TALAPRO-2 (2022): experimental 33.1 months vs control 19.5 months.
Data table
TrialYearEndpointControl (months)Experimental (months)
PROpel2022rPFS16.6 months24.8 months
TALAPRO-22022rPFS19.5 months33.1 months

First-line PARP inhibitor plus androgen-receptor drug: DNA-repair alterations

First-line metastatic castration-resistant prostate cancer with homologous recombination repair (HRR) gene alterations · Metastatic · endpoint: rPFS

Results are not comparable across trials.

MAGNITUDE's HRR-positive cohort (niraparib with abiraterone) and TALAPRO-2's HRR-deficient cohort (talazoparib with enzalutamide) used HRR definitions set by each trial, and different backbone drugs. The TALAPRO-2 median is from an updated descriptive analysis; MAGNITUDE's is from its primary analysis by central review. Follow-up differs. The BRCA subgroup results are separate analyses and are not mixed into this lane. Compare only each trial's own two arms.

Each pair shows one trial: its control arm and its experimental arm. Yesterday's experimental arm is often today's control. Populations, definitions and follow-up differ.

010203040rPFS, median (months)20222022MAGNITUDETALAPRO-2
  • experimental arm
  • control arm
  • different endpoint from the lane's
  • step line through experimental values
rPFS, median, across 2 trials in this lane. MAGNITUDE (2022): experimental 16.5 months vs control 13.7 months; TALAPRO-2 (2022): experimental 30.7 months vs control 12.3 months.
Data table
TrialYearEndpointControl (months)Experimental (months)
MAGNITUDE2022rPFS13.7 months16.5 months
TALAPRO-22022rPFS12.3 months30.7 months

Standard of care, then and now

How the usual sequence of treatment changed for one setting. Choose a point in time; each step links to the milestone behind it.

Metastatic hormone-sensitive disease: first-line treatment

Men starting androgen deprivation therapy for metastatic hormone-sensitive (castration-sensitive) prostate cancer · Metastatic

  1. Endocrine1Androgen deprivation (castration)Huggins and Hodges: hormones and prostate cancer (1941) (1941)
  2. Chemotherapy2ADT + docetaxelDocetaxel with ADT in hormone-sensitive disease (CHAARTED, STAMPEDE) (2015)
  3. Endocrine3ADT + abirateroneAbiraterone with ADT in hormone-sensitive disease (LATITUDE, STAMPEDE) (2017)
  4. Endocrine4ADT + apalutamide or enzalutamideAR inhibitors with ADT, hormone-sensitive (TITAN, ARCHES, ENZAMET) (2019)
  5. Endocrine5ADT + docetaxel + darolutamideTriplet therapy: ADT, docetaxel and an AR inhibitor (ARASENS, PEACE-1) (2022)
  6. Endocrine6ADT + darolutamide, no docetaxelDarolutamide plus ADT without docetaxel (ARANOTE) (2024)
  7. Radiation7ADT + ARPI + 177Lu-PSMA-617 (PSMA+)177Lu-PSMA-617 plus ARPI in PSMA-positive mHSPC (PSMAddition) (2026)
Today. Based only on the milestones cited in each step; not every option is shown. Darolutamide was also tested without docetaxel, and a PSMA-targeted radioligand was added for PSMA-positive disease.
Text version
  • 2004: Androgen deprivation (castration) → LHRH agonist as medical castration
  • 2015: Androgen deprivation (castration) → ADT + docetaxel
  • 2022: Androgen deprivation (castration) → ADT + docetaxel → ADT + abiraterone → ADT + apalutamide or enzalutamide → ADT + docetaxel + darolutamide
  • Today: Androgen deprivation (castration) → ADT + docetaxel → ADT + abiraterone → ADT + apalutamide or enzalutamide → ADT + docetaxel + darolutamide → ADT + darolutamide, no docetaxel → ADT + ARPI + 177Lu-PSMA-617 (PSMA+)

Metastatic castration-resistant disease: lines of treatment

Men with metastatic castration-resistant prostate cancer · Metastatic

  1. Chemotherapy1Docetaxel + prednisoneDocetaxel for castration-resistant disease (TAX 327, SWOG 9916) (2004)
  2. Chemotherapy2After docetaxel: cabazitaxelCabazitaxel after docetaxel (TROPIC) (2010)
  3. Endocrine3After docetaxel: abirateroneAbiraterone after docetaxel improves survival (COU-AA-301) (2011)
  4. Endocrine4After chemotherapy: enzalutamideEnzalutamide after docetaxel (AFFIRM) (2012)
  5. Targeted5After an ARPI: olaparib or rucaparibPARP inhibitors for HRR-altered mCRPC (PROfound, TRITON) (2020)
  6. Radiation6After ARPI and taxane: 177Lu-PSMA-617177Lu-PSMA-617 for PSMA-positive mCRPC (VISION, TheraP) (2021)
  7. Targeted7PARP inhibitor + ARPI (BRCA/HRR-altered)PARP inhibitor plus ARPI first line (PROpel, MAGNITUDE, TALAPRO-2) (2022)
  8. Radiation8Before taxane: 177Lu-PSMA-617177Lu-PSMA-617 before taxane chemotherapy (PSMAfore) (2024)
Today. Based only on the milestones cited in each step; not every option is shown. PARP inhibitors were also combined with an ARPI as first treatment, and the radioligand was tested before taxane chemotherapy.
Text version
  • 2004: Docetaxel + prednisone
  • 2012: Docetaxel + prednisone → After docetaxel: cabazitaxel → After docetaxel: abiraterone → After chemotherapy: enzalutamide
  • 2021: Docetaxel + prednisone → After docetaxel: cabazitaxel → After docetaxel: abiraterone → After chemotherapy: enzalutamide → After an ARPI: olaparib or rucaparib → After ARPI and taxane: 177Lu-PSMA-617
  • Today: Docetaxel + prednisone → After docetaxel: cabazitaxel → After docetaxel: abiraterone → After chemotherapy: enzalutamide → After an ARPI: olaparib or rucaparib → After ARPI and taxane: 177Lu-PSMA-617 → PARP inhibitor + ARPI (BRCA/HRR-altered) → Before taxane: 177Lu-PSMA-617

Today and tomorrow

Standard of care today

Screening
USPSTF recommendation page (final statement dated 8 May 2018; the page says the topic is being updated and gives no date for the update): for men aged 55 to 69 the decision to undergo periodic PSA-based screening should be an individual one (grade C), and the Task Force recommends against PSA-based screening in men aged 70 and older (grade D). FDA device actions read in the Federal Register: PSA assay premarket approvals dated 25 February 1986 (prognosis and management in people with prostate cancer) and 25 August 1994 (use with digital rectal examination as an aid in detection in men aged 50 or older). The EAU-EANM-ESTRO-ESUR-ISUP-SIOG 2026 update Part I (Eur Urol, PMID 42457454) is cited by identifier only; its text was not read, so no recommendation is attributed to it. This entry restates the USPSTF statement and is not a ranking.
US Preventive Services Task Force 2018US Preventive Services Task Force, Grossman DC, Curry SJ, Owens DK, Bibbins-Domingo K, Caughey AB, Davidson KW, et al 2018US Food and Drug Administration 1986US Food and Drug Administration 1994Guideline: Cornford P, van den Bergh RCN, Briers E, Chiu P, Eberli D, Epure A, et al 2026
Localised

FDA approval letters read for PSMA-targeted PET imaging agents, each providing for PET of PSMA-positive lesions in men with prostate cancer with suspected metastasis who are candidates for initial definitive therapy or with suspected recurrence based on elevated serum PSA:

  • Ga 68 PSMA-11 injection from the University of California Los Angeles (1 December 2020), Pylarify (26 May 2021), Illuccix (17 December 2021), Locametz (23 March 2022
  • its letter adds selection of people with metastatic prostate cancer for whom lutetium Lu 177 vipivotide tetraxetan PSMA-directed therapy is indicated) and Posluma (25 May 2023). Treatment options for localized disease (surgery, radiotherapy, active surveillance, androgen deprivation with radiotherapy) are covered in the milestone timeline. The EAU 2026 Part I and ESMO local and locoregional guidelines are cited by identifier only (PMIDs 42457454 and 41421764)
  • their text was not read
US Food and Drug Administration 2020US Food and Drug Administration 2021US Food and Drug Administration 2021US Food and Drug Administration 2022US Food and Drug Administration 2023Guideline: Cornford P, van den Bergh RCN, Briers E, Chiu P, Eberli D, Epure A, et al 2026Guideline: Walz J, Attard G, Bjartell A, Blanchard P, Castro E, Compérat E, et al 2026
Any setting

Non-metastatic disease, FDA letters and one label read. Biochemical recurrence:

  • on 16 November 2023 the FDA approved a new indication for enzalutamide for non-metastatic castration-sensitive prostate cancer with biochemical recurrence at high risk for metastasis. Non-metastatic castration-resistant disease: darolutamide on 30 July 2019 (letter: treatment of patients with non-metastatic castration-resistant prostate cancer)
  • apalutamide on 14 February 2018 (the original prescribing information lists non-metastatic castration-resistant prostate cancer
  • the replacement approval letter read does not restate the indication)
  • and a broadening of the enzalutamide indication on 13 July 2018 to castration-resistant prostate cancer, which the letter describes as proposing to broaden the indication to include both non-metastatic and metastatic disease. EAU 2026 Part II (Eur Urol, PMID 42457456) is cited by identifier only
  • its text was not read
US Food and Drug Administration 2023US Food and Drug Administration 2019US Food and Drug Administration 2018US Food and Drug Administration 2018US Food and Drug Administration 2018Guideline: Tilki D, van den Bergh RCN, Briers E, Chiu P, Eberli D, Epure A, et al 2026
Metastatic

Hormone-sensitive disease, FDA actions read (the FDA's newer term is 'metastatic androgen pathway modulation-naive or -sensitive', previously metastatic hormone-sensitive):

  • abiraterone acetate with prednisone for metastatic high-risk castration-sensitive prostate cancer (7 February 2018)
  • apalutamide, expanded to metastatic castration-sensitive prostate cancer (17 September 2019)
  • enzalutamide, revised to include metastatic castration-sensitive prostate cancer (16 December 2019)
  • darolutamide with docetaxel (5 August 2022)
  • darolutamide as a single agent for metastatic castration-sensitive prostate cancer (3 June 2025)
  • niraparib and abiraterone acetate with prednisone for BRCA2-mutated metastatic castration-sensitive prostate cancer (12 December 2025)
  • capivasertib with abiraterone and prednisone for PTEN-deficient disease, with the VENTANA PTEN (SP218) RxDx assay as companion diagnostic (12 June 2026
  • trial CAPItello-281)
  • and lutetium Lu 177 vipivotide tetraxetan with an androgen receptor pathway inhibitor for PSMA-positive disease (31 July 2026
  • trial PSMAddition
  • the corrected action letter, whose effective date remains 31 July 2026, gives the agreed indication as use in combination with ARPI therapy and has part of the proposed-indication text redacted
  • the FDA notice was also read). No FDA document on docetaxel in the hormone-sensitive setting was read. ESMO advanced and metastatic guideline (Ann Oncol, PMID 41679466) and EAU 2026 Part II (PMID 42457456) are cited by identifier only
  • their text was not read
US Food and Drug Administration 2018US Food and Drug Administration 2019US Food and Drug Administration 2019US Food and Drug Administration 2022US Food and Drug Administration 2025FDA 2025FDA 2026FDA 2026FDA 2026FDA 2026Guideline: Fizazi K, Attard G, Azad AA, Baciarello G, Beltran H, Bjartell A, et al 2026Guideline: Tilki D, van den Bergh RCN, Briers E, Chiu P, Eberli D, Epure A, et al 2026
Metastatic

Castration-resistant disease, chemotherapy, cell therapy, hormonal agents and a radiopharmaceutical, FDA documents read:

  • docetaxel with prednisone for androgen independent (hormone refractory) metastatic prostate cancer (19 May 2004)
  • sipuleucel-T licensed by the Center for Biologics Evaluation and Research, whose product page gives the indication as asymptomatic or minimally symptomatic metastatic castrate resistant (hormone refractory) prostate cancer
  • cabazitaxel with prednisone after a docetaxel-containing regimen (17 June 2010)
  • abiraterone acetate with prednisone after docetaxel (28 April 2011)
  • enzalutamide after docetaxel (31 August 2012)
  • and radium Ra 223 dichloride for castration-resistant disease with symptomatic bone metastases and no known visceral metastatic disease (15 May 2013). These dates are approval-letter dates for the indications as first granted
  • current prescribing information was not read and may differ. Later expansions of abiraterone and enzalutamide to chemotherapy-naive disease were not read. ESMO advanced and metastatic guideline (PMID 41679466) and EAU 2026 Part II (PMID 42457456) are cited by identifier only
US Food and Drug Administration 2004US Food and Drug Administration, Center for Biologics Evaluation and Research 2010US Food and Drug Administration 2010US Food and Drug Administration 2011US Food and Drug Administration 2012FDA 2013Guideline: Fizazi K, Attard G, Azad AA, Baciarello G, Beltran H, Bjartell A, et al 2026Guideline: Tilki D, van den Bergh RCN, Briers E, Chiu P, Eberli D, Epure A, et al 2026
Metastatic

Castration-resistant disease, biomarker-directed and PSMA-directed treatment, FDA letters read:

  • lutetium Lu 177 vipivotide tetraxetan for PSMA-positive disease after androgen receptor pathway inhibition and taxane-based chemotherapy (23 March 2022), with the indication revised on 28 March 2025 to people treated with an androgen receptor pathway inhibitor and considered appropriate to delay taxane chemotherapy or with prior taxane chemotherapy
  • olaparib for HRR gene-mutated disease after enzalutamide or abiraterone (19 May 2020)
  • rucaparib for BRCA-mutated disease after androgen receptor-directed therapy and a taxane under accelerated approval (15 May 2020), converted on 17 December 2025 (the letter states that approval of the supplement fulfills the commitments made under 21 CFR 314.510 and describes a new patient population treated with androgen receptor-directed therapy
  • it does not use the word 'converted')
  • olaparib with abiraterone and prednisone for BRCA-mutated disease (31 May 2023)
  • talazoparib with enzalutamide for HRR gene-mutated disease (20 June 2023)
  • and the niraparib/abiraterone acetate fixed-dose combination for BRCA-mutated disease (11 August 2023). The letters are not the current labels. Guideline text was not read
  • see the identifiers in the other metastatic entries
FDA 2022FDA 2025FDA 2020FDA 2020FDA 2025FDA 2023FDA 2023FDA 2023Guideline: Fizazi K, Attard G, Azad AA, Baciarello G, Beltran H, Bjartell A, et al 2026Guideline: Tilki D, van den Bergh RCN, Briers E, Chiu P, Eberli D, Epure A, et al 2026
Metastatic

EMA documents read (European public assessment report pages, accessed 20 October 2026):

  • sipuleucel-T (Provenge) was granted a marketing authorisation in the EU on 6 September 2013 and the European Commission withdrew it on 6 May 2015 at the request of the holder, which notified its decision to permanently discontinue marketing for commercial reasons
  • radium-223 dichloride (Xofigo) received a marketing authorisation on 13 November 2013 for castration-resistant disease with symptomatic bone metastases and no known visceral metastases, and the page states it must not be used with abiraterone acetate and prednisone or prednisolone
  • lutetium (177Lu) vipivotide tetraxetan (Pluvicto) received a marketing authorisation on 9 December 2022 and the page, last updated 20 July 2026, describes use in adults previously treated with androgen receptor pathway inhibitors and a taxane, with the pathway inhibitor optionally added. EMA indication-extension dates and other prostate cancer medicines were not read, so no European date is given for the hormone-sensitive, non-metastatic or PARP-inhibitor indications
European Medicines Agency 2015EMA 2026EMA 2026
Any setting
Androgen deprivation delivery, FDA letters read: degarelix for injection for the treatment of patients with advanced prostate cancer (24 December 2008) and the oral gonadotropin-releasing hormone receptor antagonist relugolix (Orgovyx) for the treatment of adult patients with advanced prostate cancer (18 December 2020). Original action dates for leuprolide and goserelin come from database entries only and are not listed here.
US Food and Drug Administration 2008US Food and Drug Administration 2020

Trials to watch

  • EvoPAR-Prostate01 NCT06120491

    In metastatic castration-sensitive prostate cancer, does adding saruparib to a physician's choice of new hormonal agent change radiographic progression-free survival (the registry's primary outcome) compared with placebo, in separate cohorts with and without homologous recombination repair gene mutations? Registry record: randomised phase 3, quadruple-masked, 1,898 enrolled (actual). Registry status: active, not recruiting; no results posted.

  • MEVPRO-1 NCT06551324

    In metastatic castration-resistant prostate cancer previously treated with abiraterone acetate, does mevrometostat (PF-06821497) with enzalutamide differ in radiographic progression-free survival by blinded independent central review (the registry's primary outcome) from enzalutamide or docetaxel? Registry record: randomised phase 3, open-label, 600 estimated. Registry status: active, not recruiting; no results posted.

  • OMAHA-003 (MK-5684-003) NCT06136624

    In metastatic castration-resistant prostate cancer previously treated with a next-generation hormonal agent and taxane-based chemotherapy, does opevesostat (MK-5684) differ in overall survival (the registry's primary outcomes, reported separately for androgen receptor ligand-binding-domain mutation-positive and mutation-negative participants) from alternative abiraterone acetate or enzalutamide? Registry record: randomised phase 3, open-label, 1,310 estimated. Registry status: recruiting; no results posted.

  • STAMPEDE2 NCT06320067

    In men receiving androgen deprivation therapy for metastatic prostate cancer, what is the effect on overall survival (the registry's primary outcome) of adding further treatments in this second multi-arm multi-stage platform? The registry record lists comparisons of stereotactic ablative radiotherapy (SABR) and of 177Lu-PSMA-617 against standard care. Registry record: randomised phase 3 platform, 3,360 estimated. Registry status: recruiting; no results posted.

  • DASL-HiCaP (ANZUP1801) NCT04136353

    In very high-risk, clinically localised prostate cancer, does adding darolutamide to androgen deprivation therapy and definitive or salvage radiation change metastasis-free survival (the registry's primary outcome) compared with placebo? Registry record: randomised phase 3, quadruple-masked, 1,100 enrolled (actual). Registry status: active, not recruiting; no results posted.

  • PSMA-DC NCT05939414

    In PSMA-positive oligometastatic prostate cancer, does lutetium (177Lu) vipivotide tetraxetan compared with observation change metastasis-free survival by blinded independent review (the registry's primary outcome), described in the title as delaying castration or disease recurrence? Registry record: randomised phase 3, open-label, 450 estimated. Registry status: recruiting; no results posted.

Pioneers

  • Hugh Hampton Young

    1870-1945 · Associate Professor of Genito-Urinary Surgery, The Johns Hopkins University (1905 byline)

  • Charles B. Huggins

    1901-1997 · Surgeon, Cancer researcher

  • P. C. Walsh

    Author of a 1982 paper on impotence after radical prostatectomy and first author of a 1983 report of a modified radical retropubic prostatectomy

References

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Every figure was checked against its primary source to the extent possible. Items that could not be fully confirmed are marked “needs review”. Educational history, not medical advice.

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2011TreatmentEndocrine

landmarkMetastatic

Abiraterone after docetaxel improves survival (COU-AA-301)

Abiraterone, which blocks androgen production, was tested with prednisone in 1,195 men whose metastatic castration-resistant prostate cancer had progressed after docetaxel. At the first analysis, median survival was 14.8 months with abiraterone against 10.9 months with placebo. The FDA approved it on 28 April 2011.

COU-AA-301: randomized (2:1), double-blind phase 3, n=1195, post-docetaxel mCRPC; abiraterone acetate 1000 mg plus prednisone versus placebo plus prednisone. Interim OS (median follow-up 12.8 months): 14.8 versus 10.9 months, HR 0.65 (95% CI 0.54-0.77; P<0.001). Final OS before crossover (median follow-up 20.2 months): 15.8 versus 11.2 months, HR 0.74 (0.64-0.86). Radiologic PFS 5.6 versus 3.6 months. Mineralocorticoid-related adverse events were more frequent with abiraterone.

The investigators of COU-AA-301 reasoned that biosynthesis of androgen outside the testes may contribute to progression of castration-resistant prostate cancer.[1] Abiraterone acetate inhibits androgen biosynthesis, and the trial tested it in men who had already received chemotherapy with docetaxel.[1]

The trial randomly assigned 1195 men, in a 2:1 ratio, to prednisone with abiraterone acetate 1000 mg (797 men) or with placebo (398 men).[1] At the interim analysis, after a median follow-up of 12.8 months, median overall survival was 14.8 months with abiraterone and 10.9 months with placebo, a hazard ratio for death of 0.65 (95% CI 0.54 to 0.77). Because the results exceeded the preplanned criteria for stopping, the data were unblinded.[1] Mineralocorticoid-related adverse events, including fluid retention, hypertension and hypokalemia, were reported more often with abiraterone.[1]

The FDA approved abiraterone acetate with prednisone on 28 April 2011 for metastatic castration-resistant prostate cancer after docetaxel, before the 26 May 2011 print date of the New England Journal of Medicine report.[2] The final analysis, done before crossover from placebo, reported median overall survival of 15.8 months against 11.2 months, with a hazard ratio of 0.74 (95% CI 0.64 to 0.86).[3]

Standard before

For men whose metastatic castration-resistant prostate cancer had progressed after docetaxel, the FDA had approved cabazitaxel with prednisone on 17 June 2010.

What changed

FDA approval on 28 April 2011 of abiraterone acetate with prednisone for metastatic castration-resistant prostate cancer after docetaxel.

Why it mattered

Abiraterone, an inhibitor of androgen biosynthesis, prolonged overall survival compared with placebo in men whose disease had progressed after docetaxel, and the final analysis confirmed the result.

Caveats

  • The control was placebo plus prednisone; abiraterone was not compared head to head with cabazitaxel or enzalutamide, and results from TROPIC and AFFIRM, which also followed docetaxel, are not directly comparable.
  • The final analysis was done before crossover from placebo to abiraterone, after 775 of the prespecified 797 death events.
  • The milestone year follows the FDA approval letter (28 April 2011), which precedes the 26 May 2011 print date; PubMed shows no earlier online date.