{"entity":{"id":"prostate-roadmap","kind":"roadmap","name":"Prostate cancer roadmap: from Huggins and the discovery that a cancer can depend on a hormone, through the PSA epidemic and what it cost, the androgen receptor drugs, the DNA repair subset and PSMA, to a 2032 registry watch","aka":["Prostate cancer history","Prostate cancer evidence roadmap","History of prostate cancer treatment","Prostate cancer timeline"],"tldr":"Prostate cancer is where hormone therapy for cancer was invented, in 1941, and where a blood test created an epidemic of diagnoses forty-five years later. This roadmap follows the evidence from castration to the modern androgen receptor drugs, through the screening trials and the argument about overdiagnosis they started, to DNA repair, PSMA and the questions still open in 2032.","summary":"In 1941 Charles Huggins and Clarence Hodges castrated men with advanced prostate cancer and watched the disease regress. It was the first demonstration that any human cancer depends on a circulating hormone, and it is still the backbone of treatment: every man who starts androgen deprivation is repeating the experiment. What followed was a long argument about how to do the same thing better, and it turned out that castration resistance is not the cancer ignoring the hormone but adapting to live on less of it. Visakorpi found amplified androgen receptor in a third of recurrent tumours in 1995; Chen showed in 2004 that receptor overexpression alone converts sensitive disease to resistant and turns antagonists into agonists; Attard's 2008 phase 1 of abiraterone proved the point in people, and enzalutamide, built to the specification Chen described, followed.\n\nThe other half of the story is detection. Stamey described prostate-specific antigen as a marker in 1987 and Catalona made it a screening test in 1991, with the 4.0 threshold still on laboratory reports today. Testing spread through primary care before any trial had asked whether it saved lives. When the trials reported in 2009 they disagreed: ERSPC found a 20 percent reduction in prostate cancer mortality at a cost of 1,410 men screened and 48 extra cancers treated per death prevented, and PLCO found nothing, largely because half its control group was being screened anyway. Welch and Albertsen counted what had happened in the meantime: 1.3 million extra American men diagnosed and about a million treated. The United States task force recommended against screening in 2012 and partly reversed itself in 2018.\n\nTreatment moved in the 2000s and then very fast in the 2010s. Docetaxel in 2004 was the first drug to extend survival in castration-resistant disease; cabazitaxel opened the second line in 2010; abiraterone and enzalutamide moved from post-chemotherapy to pre-chemotherapy and then, through CHAARTED, STAMPEDE, LATITUDE, TITAN, ENZAMET, ARASENS and PEACE-1, to the first day of metastatic diagnosis. The genome was mapped in parallel: the TMPRSS2-ERG fusion in 2005, the TCGA taxonomy and the SU2C metastatic cohort in 2015, and the finding that made the biggest practical difference, DNA repair gene alterations in about a fifth of advanced tumours, with 11.8 percent of men carrying an inherited one whatever their family history. PARP inhibitors followed, and PSMA, a protein on the surface of almost every prostate cancer cell, became first an imaging target and then a way of delivering radiation to it.\n\nWhat has not been solved is stated plainly in the open problems on the prostate cancer page. Overdiagnosis is real and unquantified to within a factor of thirty. Nobody knows in what order to give the treatments that now exist. Resistance arrives for all of them, and in a minority the cancer stops being prostate cancer in any recognisable sense and becomes neuroendocrine, for which there is nothing. And a disease that mostly affects older men has its biggest remaining mortality gap in the causes of death that are not cancer.\n\nUK and NHS specifics (the National Screening Committee position, NICE technology appraisals and their recommendation numbers, Cancer Drugs Fund status, magnetic resonance imaging and radiotherapy capacity, National Prostate Cancer Audit indicators and trial access) belong on the UK and NHS page for prostate cancer and are not restated here.","status":"active","asOf":"2026-09-25","links":[{"label":"NCI PDQ: prostate cancer","url":"https://www.cancer.gov/types/prostate"},{"label":"ESMO guidelines: prostate cancer","url":"https://www.esmo.org/guidelines/esmo-clinical-practice-guidelines-genitourinary-cancers/prostate-cancer"},{"label":"EAU guidelines: prostate cancer","url":"https://uroweb.org/guidelines/prostate-cancer"},{"label":"ClinicalTrials.gov NCT06320067","url":"https://clinicaltrials.gov/study/NCT06320067"}],"tags":[],"related":["hormonal-therapy-roadmap","early-detection-roadmap","targeted-therapy-roadmap","radiopharma-roadmap","molecular-imaging-roadmap","surgery-roadmap","chemotherapy-roadmap","immunotherapy-roadmap","diagnostics-roadmap"],"cancers":["prostate","prostate-low-risk","prostate-intermediate-risk","prostate-high-risk","prostate-bcr","prostate-mhspc","prostate-nmcrpc","prostate-mcrpc","prostate-nepc"],"sections":["hormonal","early-detection","diagnostics","targeted-therapy","radiopharma","surgery","chemotherapy","imaging"],"technologies":[],"targets":[],"drugs":[],"companies":[],"institutions":[],"pathways":[],"terms":[],"trials":[],"people":[],"bottlenecks":["b-overdiagnosis","b-early-detection","b-resistance","b-biomarker-validation","b-hereditary-risk","b-toxicity-qol","b-immunotherapy-response","b-trial-design","b-global-access","b-survivorship"],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"steps":[{"era":"1941 to 1966","title":"A cancer is shown to depend on a hormone, and systemic cancer therapy begins","description":"Huggins and Hodges measured serum phosphatases in men with metastatic prostate cancer, then castrated them or gave them oestrogen and watched the disease regress; androgen injection sent it the other way. No cancer in any organ had previously been made to shrink by anything other than surgery or radiation. Huggins shared the 1966 Nobel Prize for it. High-dose oestrogen was the first medical castration and was abandoned for cardiovascular harm rather than for lack of effect, which is why luteinising hormone-releasing hormone agonists replaced it and why transdermal oestradiol, which avoids first-pass hepatic effects, is still being tested as an alternative.","refs":["paper-huggins-hodges-castration-serum-phosphatases-prostate-1941","paper-langley-lancet","hormonal-therapy-roadmap"],"status":"historic"},{"era":"1987 to 2005","title":"A blood test arrives, and an epidemic of diagnoses follows it","description":"Stamey described prostate-specific antigen as a marker that tracked tumour volume, fell to nothing after prostatectomy and rose again on recurrence, and stated in the same paper that it is not specific. Catalona turned it into a screening test in 1991 with a threshold of 4.0 micrograms per litre and showed it found cancers a digital rectal examination missed. Testing spread through United States primary care over the following decade without a randomised trial of mortality. By 2005 the consequence was measurable: relative incidence against 1986 was 7.23 in men under 50 and 0.56 in men aged 80 and over, an extra 1,305,600 diagnoses and 1,004,800 definitive treatments.","refs":["paper-stamey-psa-serum-marker-nejm-1987","paper-catalona-psa-screening-test-nejm-1991","paper-welch-albertsen-psa-era-diagnosis-treatment-jnci-2009","paper-damico-risk-groups-jama-1998","early-detection-roadmap"],"status":"historic"},{"era":"1989 to 2023","title":"Does treating localised disease help? Three trials, three answers, one rule","description":"SPCG-4 randomised 695 men with clinically detected cancer from 1989 and found, at 29 years, that surgery cut prostate cancer death by 45 percent and added a mean of 2.9 years of life. PIVOT randomised a largely prostate-specific antigen-detected population from 1994 and found no significant difference at 19.5 years, with more incontinence and sexual dysfunction and less treatment for biochemical progression. ProtecT randomised men found by screening and, at 15 years, found prostate cancer mortality of around 3 percent in all three arms. The rule those three produce is the one that matters at diagnosis: how much radical treatment helps depends on how the cancer was found and how aggressive it is, and a Gleason score above 7 carried ten times the risk of death of a score of 6 or lower in SPCG-4.","refs":["paper-bill-axelson-spcg-4-29-year-nejm-2018","paper-wilt-pivot-prostatectomy-observation-nejm-2017","paper-protect-nejm-2016","paper-protect-15-year-nejm-2023","paper-klotz-active-surveillance-jco-2015","surgery-roadmap"],"status":"historic"},{"era":"2009 to 2018","title":"The screening trials disagree, and the policy swings twice","description":"ERSPC randomised 162,243 men in its core age group and found a rate ratio for prostate cancer death of 0.80, an absolute difference of 0.71 death per 1,000 men, 1,410 to screen and 48 extra cancers to treat for each death prevented, and cumulative incidence of 8.2 percent against 4.8. PLCO, published the same day, found no difference, with control-group screening rising to 52 percent by year six. The United States task force issued a grade D recommendation against screening in 2012 and in 2018 moved men aged 55 to 69 to grade C, shared decision-making, quoting about 1.3 deaths and about 3 metastatic cases prevented per 1,000 men screened against 1 in 5 developing long-term incontinence and 2 in 3 long-term erectile dysfunction after prostatectomy. The modelling work that ran alongside showed why a single overdiagnosis figure is not meaningful: lead time of 5.4 to 6.9 years and overdiagnosis of 23 to 42 percent in the United States calibration, 7.9 years and 66 percent in the Rotterdam one.","refs":["paper-schroder-erspc-screening-mortality-nejm-2009","paper-andriole-plco-prostate-screening-nejm-2009","paper-draisma-lead-time-overdiagnosis-psa-jnci-2009","paper-moyer-uspstf-prostate-screening-ann-intern-med-2012","paper-uspstf-prostate-screening-jama-2018","paper-hugosson-eur-urol","paper-martin-jama"],"status":"historic"},{"era":"2004 to 2014","title":"Chemotherapy works, a little, and then the receptor drugs arrive","description":"TAX 327 and SWOG 9916, published in the same issue in October 2004, both showed docetaxel extends survival in castration-resistant disease, by 2.4 and 1.9 months respectively over mitoxantrone, and TAX 327 also improved pain and quality of life. TROPIC opened the second line in 2010 with cabazitaxel, 15.1 against 12.7 months. Then the hormonal drugs designed on the Visakorpi and Chen biology arrived: abiraterone after chemotherapy in COU-AA-301 and before it in COU-AA-302, enzalutamide after chemotherapy in AFFIRM (18.4 against 13.6 months) and before it in PREVAIL (radiographic progression-free survival 65 percent against 14 percent at 12 months). Within four years castration-resistant prostate cancer went from one treatment to five.","refs":["paper-tannock-tax-327-docetaxel-prednisone-nejm-2004","paper-petrylak-swog-9916-docetaxel-estramustine-nejm-2004","paper-de-bono-tropic-cabazitaxel-lancet-2010","paper-cou-aa-301-abiraterone-de-bono-nejm-2011","paper-abiraterone-acetate-prostate-n-engl-j-med-2013","paper-scher-affirm-enzalutamide-nejm-2012","paper-beer-prevail-enzalutamide-nejm-2014","paper-alsympca-radium-223-nejm-2013","chemotherapy-roadmap"],"status":"historic"},{"era":"2005 to 2016","title":"The genome: a quiet sequence, a rearranged structure, and one actionable fifth","description":"Tomlins found the TMPRSS2-ERG fusion in 2005, the first recurrent rearrangement in a common carcinoma, putting a growth gene under androgen control. Taylor showed copy-number pattern separates risk better than Gleason score. Grasso sequenced 50 lethal cancers at rapid autopsy and found only 2.00 mutations per megabase even after years of treatment, with the recurrent damage in chromatin-modifying genes. Baca named chromoplexy, chains of rearrangement arriving in a burst. In 2015 TCGA classified 333 primary tumours into seven subtypes covering 74 percent of them, and the Stand Up To Cancer cohort sequenced 150 metastatic biopsies prospectively and found DNA repair alterations in 19.3 percent. Gundem reconstructed how the cancer travels and found that metastases seed other metastases, often several clones at a time. Pritchard then showed 11.8 percent of men with metastatic disease carry an inherited DNA repair mutation, with no relation to family history or age.","refs":["paper-tomlins-tmprss2-ets-fusion-science-2005","paper-taylor-integrative-genomic-profiling-cancer-cell-2010","paper-grasso-mutational-landscape-lethal-crpc-nature-2012","paper-baca-punctuated-evolution-chromoplexy-cell-2013","paper-tcga-molecular-taxonomy-primary-prostate-cell-2015","paper-robinson-integrative-clinical-genomics-advanced-prostate-cell-2015","paper-gundem-evolutionary-history-lethal-metastatic-prostate-nature-2015","paper-pritchard-inherited-dna-repair-metastatic-prostate-nejm-2016"],"status":"historic"},{"era":"2013 to 2022","title":"Everything moves to the first day of metastatic diagnosis","description":"GETUG-AFU 15 gave docetaxel with androgen deprivation from the start and found nothing, and told the field not to do it. CHAARTED and STAMPEDE then found the opposite, and the STOpCaP adaptive meta-analysis resolved the three: in metastatic disease, a hazard ratio of 0.77 and an absolute 9 percent gain in four-year survival, with no evidence of benefit from zoledronic acid at all. LATITUDE and STAMPEDE did the same for abiraterone, TITAN for apalutamide, ENZAMET for enzalutamide, and ARASENS and PEACE-1 established the triplet of androgen deprivation, docetaxel and an androgen receptor pathway inhibitor. STAMPEDE also showed that irradiating the prostate itself improves survival in men with a low burden of metastases. In non-metastatic castration-resistant disease, SPARTAN, PROSPER and ARAMIS moved the same class earlier again.","refs":["paper-gravis-getug-afu-15-docetaxel-lancet-oncol-2013","paper-chaarted-nejm-2015","paper-stampede-lancet-2016","paper-vale-stopcap-docetaxel-bisphosphonates-lancet-oncol-2016","paper-latitude-nejm-2017","paper-stampede-abiraterone-nejm-2017","paper-nct02489318-n-engl-j-med-2019","paper-enzamet-n-engl-j-med-2019","paper-arasens-nejm-2022","paper-peace-1-lancet-2022","paper-parker-lancet","paper-spartan-nejm-2018","paper-prosper-nejm-2018","paper-aramis-nejm-2019"],"status":"current"},{"era":"2015 to 2026","title":"DNA repair: the first molecular subset of prostate cancer with a drug of its own","description":"TOPARP-A treated 50 unselected heavily pre-treated men with olaparib and biopsied all of them: 33 percent responded, and 14 of the 16 men with DNA repair defects did, including all 7 with BRCA2 loss, at a biomarker specificity of 94 percent. PROfound made it randomised, TRITON2 got rucaparib approved on response rate and TRITON3 confirmed it, with imaging-based progression-free survival of 11.2 against 6.4 months in the BRCA subgroup and a hazard ratio of 0.95 in the ATM subgroup, which is no effect at all. PROpel, TALAPRO-2 and MAGNITUDE then combined PARP inhibitors with androgen receptor drugs in first-line castration-resistant disease, and TALAPRO-3 and AMPLITUDE have moved the combination into hormone-sensitive disease. The recurring lesson is that homologous recombination repair is not one biomarker: BRCA2 is not ATM and neither is CDK12.","refs":["paper-mateo-toparp-a-olaparib-dna-repair-nejm-2015","paper-profound-nejm-2020","paper-abida-triton2-rucaparib-brca-jco-2020","paper-fizazi-triton3-rucaparib-nejm-2023","paper-propel-lancet-oncol-2023","paper-talapro-2-lancet-2023","paper-magnitude-j-clin-oncol-2023","paper-nct04497844-nat-med-2025","paper-nct04821622-n-engl-j-med-2026","paper-chung-comprehensive-genomic-profiling-prostate-jco-po-2019","targeted-therapy-roadmap"],"status":"current"},{"era":"2017 to 2026","title":"PSMA: the same molecule used to see the cancer and then to irradiate it","description":"Prostate-specific membrane antigen sits on the surface of almost every prostate cancer cell, which makes it both a camera target and a delivery address. proPSMA showed PSMA positron emission tomography beats conventional imaging for staging high-risk disease, changing management in a substantial minority. TheraP compared lutetium-177 PSMA-617 against cabazitaxel and VISION added it to standard care after an androgen receptor drug and a taxane. PSMAfore moved it in front of the taxane and PSMAddition into hormone-sensitive disease. It is the clearest example in any solid tumour of a single molecule carrying both the diagnostic and the therapeutic, and the open question is dosing: the amount of radiation delivered is not currently measured per patient, and the schedule is fixed rather than adapted to response.","refs":["paper-propsma-hofman-lancet-2020","paper-psma-prerp-hope-jama-oncol-2021","paper-therap-lancet-2021","paper-vision-nejm-2021","paper-psmafore-lancet-2024","paper-psmaddition-lancet-2026","radiopharma-roadmap","molecular-imaging-roadmap"],"status":"current"},{"era":"2014 to 2026","title":"What the androgen receptor era created: splice variants, lineage switching and a cold tumour","description":"Antonarakis showed in 2014 that men whose circulating tumour cells carry AR-V7, an androgen receptor missing the part the drugs bind, have a zero percent prostate-specific antigen response rate to enzalutamide and abiraterone. Mu and Ku then showed the more complete escape: losing TP53 and RB1 lets the cell switch on SOX2 and change identity from a luminal cell that needs the androgen receptor to a basal or neuroendocrine cell that does not, and restoring the tumour suppressors reverses it in the laboratory. Aggarwal found treatment-emergent small-cell neuroendocrine carcinoma in 17 percent of metastatic biopsies. Immunotherapy, which might have been the answer, is not: KEYNOTE-199 gave response rates of 5 and 3 percent and PD-L1 expression predicted nothing, which is consistent with a median tumour mutational burden of 2.6 mutations per megabase and mismatch repair deficiency in 4 percent.","refs":["paper-antonarakis-ar-v7-resistance-nejm-2014","paper-mu-sox2-lineage-plasticity-science-2017","paper-ku-science","paper-beltran-nepc-divergent-evolution-nat-med-2016","paper-aggarwal-t-sccpc-jco-2018","paper-antonarakis-keynote-199-pembrolizumab-jco-2020","paper-chung-comprehensive-genomic-profiling-prostate-jco-po-2019"],"status":"emerging"},{"era":"2018 to 2030","title":"Reversing the adaptation instead of blocking it, and asking what order to give things in","description":"RESTORE gave supraphysiological testosterone to men who had progressed on enzalutamide: 30 percent responded, and 52 percent of those who then went back on enzalutamide responded to the drug that had failed them. TRANSFORMER randomised the approach and found the primary endpoint flat at 5.7 months in both arms, but progression-free survival through crossover of 28.2 months for testosterone-then-enzalutamide against 19.6 for the reverse, with quality of life favouring testosterone throughout. SWOG 9346 had already shown that taking planned breaks from androgen deprivation is not clearly safe, with a hazard ratio of 1.10 whose confidence interval crossed the non-inferiority boundary. Between them these three trials make the same point from different directions: in a disease with six active treatment classes and no head-to-head sequencing data, the order is itself an untested intervention.","refs":["paper-teply-restore-bipolar-androgen-therapy-lancet-oncol-2018","paper-denmeade-transformer-bipolar-androgen-therapy-jco-2021","paper-hussain-swog-9346-intermittent-androgen-deprivation-nejm-2013","paper-zhang-nat-commun","idea-bio1-alternating-schedules","idea-tr1-adaptive-therapy-randomised-phase-2"],"status":"emerging"},{"era":"2026 to 2032","title":"What would have to be true for prostate cancer mortality to fall substantially again","description":"Five things, only one of which is a new drug. A screening pathway judged on metastatic presentation rather than on incidence, invited by risk rather than by birthday, with magnetic resonance imaging in front of the biopsy so the overdiagnosis half of the trade shrinks. DNA repair testing at the moment of metastatic diagnosis rather than three lines later, because the drugs have already moved there. The order of treatment randomised, in a platform that can compare sequences rather than only drugs. Lineage plasticity watched for in the men whose tumours have lost TP53 and RB1, before the biopsy comes back neuroendocrine. And the mortality gap that survives equal access, which is dying of something other than prostate cancer, measured and treated as an outcome of the cancer service rather than someone else's problem.","refs":["idea-prostate-metastatic-presentation-as-the-screening-endpoint","idea-prostate-hrr-testing-at-metastatic-diagnosis","idea-prostate-randomise-the-sequence-not-only-the-drugs","idea-prostate-plasticity-surveillance-before-it-is-neuroendocrine","idea-prostate-other-cause-mortality-as-a-reported-service-outcome","idea-prostate-per-lesion-mri-audit-before-focal-treatment","idea-prostate-bipolar-androgen-therapy-phase-3-on-pfs2"],"status":"speculative"}],"watch":[{"item":"ProBio: the biomarker-driven outcome-adaptive platform in metastatic prostate cancer, the first trial designed to compare treatment strategies rather than single drugs in this disease","expected":"Primary completion and study completion December 2026 (estimated, ClinicalTrials.gov NCT03903835)","source":"https://clinicaltrials.gov/study/NCT03903835","refs":["idea-prostate-randomise-the-sequence-not-only-the-drugs"]},{"item":"PSMAddition: lutetium-177 PSMA-617 added to standard care in metastatic hormone-sensitive disease, the earliest setting radioligand therapy has been tested in","expected":"Study completion 11 February 2027 (estimated; primary completion 13 January 2025 actual, ClinicalTrials.gov NCT04720157)","source":"https://clinicaltrials.gov/study/NCT04720157","refs":["paper-psmaddition-lancet-2026","psmaddition"]},{"item":"CAPItello-281: capivasertib with abiraterone in PTEN-deficient metastatic hormone-sensitive disease, the first PI3K-pathway result in a biomarker-selected prostate population","expected":"Study completion 31 March 2027 (estimated; primary completion 7 October 2024 actual, ClinicalTrials.gov NCT04493853)","source":"https://clinicaltrials.gov/study/NCT04493853","refs":["paper-capitello-281-ann-oncol-2026","capitello-281","paper-tcga-molecular-taxonomy-primary-prostate-cell-2015"]},{"item":"TALAPRO-3: talazoparib with enzalutamide in DNA damage repair gene-mutated metastatic hormone-sensitive disease, the PARP combination moved to the hormone-sensitive setting","expected":"Study completion 28 August 2027 (estimated; primary completion 18 February 2026 actual, ClinicalTrials.gov NCT04821622)","source":"https://clinicaltrials.gov/study/NCT04821622","refs":["paper-nct04821622-n-engl-j-med-2026","nct04821622","idea-prostate-hrr-testing-at-metastatic-diagnosis"]},{"item":"PROTEUS: perioperative apalutamide with androgen deprivation around radical prostatectomy in high-risk localised disease, the largest test of intensification before the operation","expected":"Primary completion 1 December 2026 and study completion 13 October 2028 (both estimated, ClinicalTrials.gov NCT03767244)","source":"https://clinicaltrials.gov/study/NCT03767244","refs":["paper-nct03767244-n-engl-j-med-2026","nct03767244"]},{"item":"PEACE III: radium-223 with enzalutamide against enzalutamide alone in bone-metastatic castration-resistant disease, and the bone-protecting agent question it raised","expected":"Study completion December 2028 (estimated; primary completion 19 February 2024 actual, ClinicalTrials.gov NCT02194842)","source":"https://clinicaltrials.gov/study/NCT02194842","refs":["paper-alsympca-radium-223-nejm-2013","paper-lutetium-177-vipivotide-tetrax-prostate-oncol-ther-2025"]},{"item":"PSMA-DC: lutetium-177 vipivotide tetraxetan against observation in oligometastatic castration-sensitive disease detected on PSMA imaging, the test of whether a systemic radioligand can replace metastasis-directed treatment","expected":"Primary completion 25 April 2028 and study completion 3 October 2031 (both estimated, ClinicalTrials.gov NCT05939414)","source":"https://clinicaltrials.gov/study/NCT05939414","refs":["nct05939414","paper-phillips-jama-oncol","idea-psma-pet-guided-mdt"]},{"item":"STAMPEDE2: the successor platform, testing stereotactic radiotherapy to metastases, lutetium-177 PSMA-617 and niraparib with abiraterone against contemporary standard care, with 3,360 men planned","expected":"Primary completion April 2031 and study completion March 2032 (both estimated, ClinicalTrials.gov NCT06320067)","source":"https://clinicaltrials.gov/study/NCT06320067","refs":["stampede","paper-stampede-abiraterone-high-risk-attard-lancet-2022","idea-prostate-randomise-the-sequence-not-only-the-drugs"]}]},"route":"/roadmaps/prostate-roadmap/","neighbours":{"roadmap":[{"id":"chemotherapy-roadmap","kind":"roadmap","name":"Chemotherapy roadmap: mustard gas → curative combinations → the warhead inside smarter drugs","route":"/roadmaps/chemotherapy-roadmap/"},{"id":"ctdna-tests","kind":"roadmap","name":"ctDNA tests roadmap: from a curiosity in plasma to blood tests that decide treatment","route":"/roadmaps/ctdna-tests/"},{"id":"diagnostics-roadmap","kind":"roadmap","name":"Diagnostics roadmap: stains → gene panels → blood tests that decide treatment","route":"/roadmaps/diagnostics-roadmap/"},{"id":"early-detection-roadmap","kind":"roadmap","name":"Early detection roadmap: organ screening → blood tests for many cancers","route":"/roadmaps/early-detection-roadmap/"},{"id":"hormonal-therapy-roadmap","kind":"roadmap","name":"Hormonal therapy roadmap: removing the ovaries → tamoxifen → oral degraders switched by a blood test","route":"/roadmaps/hormonal-therapy-roadmap/"},{"id":"immunotherapy-roadmap","kind":"roadmap","name":"Immunotherapy roadmap: Coley's toxins → checkpoint inhibitors → engineered immunity","route":"/roadmaps/immunotherapy-roadmap/"},{"id":"molecular-imaging-roadmap","kind":"roadmap","name":"Molecular imaging roadmap: FDG → PSMA → FAP → antigen and immune PET","route":"/roadmaps/molecular-imaging-roadmap/"},{"id":"radiopharma-roadmap","kind":"roadmap","name":"Radiopharmaceutical roadmap: iodine → lutetium → actinium","route":"/roadmaps/radiopharma-roadmap/"},{"id":"survivorship-roadmap","kind":"roadmap","name":"Supportive care and survivorship roadmap: making treatment bearable → proving it extends life → caring for tens of millions afterwards","route":"/roadmaps/survivorship-roadmap/"},{"id":"surgery-roadmap","kind":"roadmap","name":"Surgery roadmap: radical operations → less surgery → no surgery when a drug has done the work","route":"/roadmaps/surgery-roadmap/"},{"id":"targeted-therapy-roadmap","kind":"roadmap","name":"Targeted therapy roadmap: imatinib → designed for resistance → the undruggable drivers fall","route":"/roadmaps/targeted-therapy-roadmap/"},{"id":"trial-modernisation-roadmap","kind":"roadmap","name":"Trial modernisation roadmap: the randomised trial → platforms and adaptive designs → decentralised, pragmatic and always-on","route":"/roadmaps/trial-modernisation-roadmap/"}],"cancer":[{"id":"prostate-bcr","kind":"cancer","name":"Biochemical recurrence of prostate cancer","route":"/cancers/prostate-bcr/"},{"id":"prostate-high-risk","kind":"cancer","name":"Localised prostate cancer, high and very high risk","route":"/cancers/prostate-high-risk/"},{"id":"prostate-intermediate-risk","kind":"cancer","name":"Localised prostate cancer, intermediate risk","route":"/cancers/prostate-intermediate-risk/"},{"id":"prostate-low-risk","kind":"cancer","name":"Localised prostate cancer, very low and low risk","route":"/cancers/prostate-low-risk/"},{"id":"prostate-mcrpc","kind":"cancer","name":"Metastatic castration-resistant prostate cancer","route":"/cancers/prostate-mcrpc/"},{"id":"prostate-mhspc","kind":"cancer","name":"Metastatic hormone-sensitive prostate cancer","route":"/cancers/prostate-mhspc/"},{"id":"prostate-nepc","kind":"cancer","name":"Neuroendocrine and small-cell prostate 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decide","route":"/ideas/idea-prev-prostate-as-triggered-biopsy/"},{"id":"idea-psma-pet-guided-mdt","kind":"idea","name":"PSMA-PET-guided metastasis-directed therapy as a curative strategy in oligorecurrent prostate cancer","route":"/ideas/idea-psma-pet-guided-mdt/"},{"id":"idea-prostate-per-lesion-mri-audit-before-focal-treatment","kind":"idea","name":"Publish a per-lesion miss rate for every prostate MRI service before it is allowed to guide focal treatment","route":"/ideas/idea-prostate-per-lesion-mri-audit-before-focal-treatment/"},{"id":"idea-prostate-randomise-the-sequence-not-only-the-drugs","kind":"idea","name":"Randomise the order of treatment, not only the drugs: a strategy platform for metastatic prostate cancer","route":"/ideas/idea-prostate-randomise-the-sequence-not-only-the-drugs/"},{"id":"idea-prostate-other-cause-mortality-as-a-reported-service-outcome","kind":"idea","name":"Report death from other causes as an outcome of the prostate cancer service, split by deprivation and ethnicity","route":"/ideas/idea-prostate-other-cause-mortality-as-a-reported-service-outcome/"},{"id":"idea-bio1-alternating-schedules","kind":"idea","name":"Rotate between drugs on a fixed schedule instead of waiting for failure","route":"/ideas/idea-bio1-alternating-schedules/"},{"id":"idea-tr1-smart-designs-for-adaptive-strategies","kind":"idea","name":"SMART designs to test treatment strategies, not just single drugs","route":"/ideas/idea-tr1-smart-designs-for-adaptive-strategies/"},{"id":"idea-prostate-bipolar-androgen-therapy-phase-3-on-pfs2","kind":"idea","name":"Take high-dose testosterone to phase 3, with progression-free survival through the second line as the primary endpoint","route":"/ideas/idea-prostate-bipolar-androgen-therapy-phase-3-on-pfs2/"},{"id":"idea-prostate-hrr-testing-at-metastatic-diagnosis","kind":"idea","name":"Test every man for DNA repair faults on the day his prostate cancer is found to have spread, not three treatments later","route":"/ideas/idea-prostate-hrr-testing-at-metastatic-diagnosis/"},{"id":"idea-prev-gleason6-terminology-rct","kind":"idea","name":"Test whether calling Gleason 6 'not cancer' changes what men choose","route":"/ideas/idea-prev-gleason6-terminology-rct/"},{"id":"idea-prev-prs-screening-start-age","kind":"idea","name":"Use a polygenic risk score to set when screening starts","route":"/ideas/idea-prev-prs-screening-start-age/"},{"id":"idea-prostate-plasticity-surveillance-before-it-is-neuroendocrine","kind":"idea","name":"Watch for the cancer changing cell type before the biopsy says neuroendocrine, and act on it","route":"/ideas/idea-prostate-plasticity-surveillance-before-it-is-neuroendocrine/"}]}}