{"entity":{"id":"prostate","kind":"cancer","name":"Prostate cancer","aka":["Prostatic acinar adenocarcinoma","Acinar adenocarcinoma of the prostate","Adenocarcinoma of the prostate","Prostate carcinoma","Carcinoma of the prostate","CaP"],"tldr":"Prostate cancer is the home of theranostics: PSMA PET finds it, PSMA radioligands treat it. Hormonal therapy remains the foundation, with PARP and AKT inhibitors added by genotype.","summary":"Prostate cancer is the most common cancer in men in most high-income countries and a spectrum: most PSA-detected disease is indolent and safely watched (ProtecT: ~3% prostate-cancer mortality at 15 years whatever the strategy), while de novo metastatic disease, treated with hormonal doublets and triplets and since 2026 with radioligand therapy added, has a median overall survival of about five years in the trial populations behind those regimens, which means half of those men lived longer; it is the second most common cause of cancer death in men. Diagnosis now runs PSA → multiparametric MRI (PRECISION) → targeted biopsy → Grade Group, with germline and somatic HRR testing for advanced disease and PSMA PET for staging (proPSMA) and recurrence. Digital-pathology AI (ArteraAI Prostate, 2025) and gene-expression classifiers (Decipher) refine who needs treatment and who benefits from adding hormone therapy.\n\nTreatment is built on androgen deprivation, the first targeted cancer therapy (Huggins, 1941). Metastatic hormone-sensitive disease is treated with doublets (ADT + abiraterone, enzalutamide, apalutamide or darolutamide) or triplets adding docetaxel (ARASENS, PEACE-1), and since 31 July 2026 with 177Lu-PSMA-617 added to ADT + ARPI (PSMAddition, rPFS HR 0.72). PTEN-deficient disease gained capivasertib + abiraterone in 2026. In castration-resistant disease the sequence includes ARPI switch, PARP inhibitors for HRR-mutant tumours (PROfound, PROpel, TALAPRO-2 with OS benefit), docetaxel and cabazitaxel, radium-223 for bone-only disease, and 177Lu-PSMA-617 before or after chemotherapy (VISION, PSMAfore). Enzalutamide is approved even for high-risk PSA-only recurrence (EMBARK).\n\nProstate cancer is the proving ground for theranostics: PSMA PET selects and PSMA radioligands treat. Competing 177Lu-PSMA-I&T products (SPLASH, ECLIPSE) have improved progression but not yet survival; alpha-emitting 225Ac-PSMA agents are in phase 3 (AlphaBreak, AcTION) and produce responses after lutetium failure. T-cell engagers against STEAP1 (xaluritamig, XALute) and KLK2 (pasritamig) are the first immunotherapies with real activity in a disease that ignores checkpoint inhibitors; EZH2 inhibition (mevrometostat, MEVPRO) aims to re-sensitise to hormonal therapy. The unsolved problems are neuroendocrine transformation, AR-V7-driven resistance (the N-terminal-domain inhibitor masofaniten failed), Ac-225 supply, and the over- versus under-diagnosis tension in screening.","asOf":"2026-09-25","wikipedia":"https://en.wikipedia.org/wiki/Prostate_cancer","links":[{"label":"Wikipedia","url":"https://en.wikipedia.org/wiki/Prostate_cancer"},{"label":"NCCN Guidelines: Prostate Cancer","url":"https://www.nccn.org/guidelines/guidelines-detail?category=1&id=1459"},{"label":"NICE NG131: prostate cancer, diagnosis and management (recommendations, including the Cambridge Prognostic Group table at 1.2.15)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"},{"label":"Royal College of Pathologists G084: dataset for histopathology reports for prostatic carcinoma, version 4, October 2024","url":"https://www.rcpath.org/static/8cc88604-2c8d-4df4-a99542df41c102af/G084-dataset-for-histopathology-reports-for-prostatic-carcinoma.pdf"},{"label":"WHO Classification of Tumours, 5th edition: tumours of the prostate (IARC, 2022)","url":"https://tumourclassification.iarc.who.int/chapters/36"},{"label":"Kench et al., Histopathology 2022: WHO Classification of Tumours fifth edition, evolving issues in the classification, diagnosis and prognostication of prostate cancer","url":"https://doi.org/10.1111/his.14711"},{"label":"Brierley et al., International Journal of Cancer 2026: the 9th edition of the UICC TNM classification of malignant tumours, updates and rationale for change (prostate at section 10.1)","url":"https://doi.org/10.1002/ijc.70561"},{"label":"UICC: the 9th edition of the TNM classification of malignant tumours, published 3 July 2025 and recommended to take effect from 1 January 2026","url":"https://www.uicc.org/news-and-updates/25-7-announcements/9th-edition-uicc-tnm-classification-malignant-tumours-now-available"},{"label":"GLOBOCAN prostate fact sheet (IARC Global Cancer Observatory, 2024 estimates)","url":"https://gco.iarc.who.int/media/globocan/factsheets/cancers/27-prostate-fact-sheet.pdf"},{"label":"SEER Cancer Stat Facts: prostate cancer (US incidence, stage distribution and survival by stage)","url":"https://seer.cancer.gov/statfacts/html/prost.html"},{"label":"Cancer Research UK: prostate cancer statistics (UK incidence, mortality, survival, stage at diagnosis and route to diagnosis)","url":"https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/prostate-cancer"},{"label":"NHS: symptoms of prostate cancer, and what happens at the GP appointment","url":"https://www.nhs.uk/conditions/prostate-cancer/symptoms/"},{"label":"Ranasinha et al., BJUI Compass 2021: ductal adenocarcinoma of the prostate, a systematic review and meta-analysis of incidence, presentation, prognosis and management","url":"https://doi.org/10.1002/bco2.60"},{"label":"Netto et al., European Urology 2022: the 2022 WHO classification of tumours of the urinary system and male genital organs, part B (prostate and urinary tract)","url":"https://pubmed.ncbi.nlm.nih.gov/35965208/"},{"label":"Epstein et al., American Journal of Surgical Pathology 2016: the 2014 ISUP consensus conference on Gleason grading, and the grade group system","url":"https://doi.org/10.1097/PAS.0000000000000530"},{"label":"NHS: prostate cancer","url":"https://www.nhs.uk/conditions/prostate-cancer/"},{"label":"NHS: tests and next steps for prostate cancer","url":"https://www.nhs.uk/conditions/prostate-cancer/tests-and-next-steps/"},{"label":"NHS: treatment for prostate cancer","url":"https://www.nhs.uk/conditions/prostate-cancer/treatment/"},{"label":"NHS: help and support for prostate cancer","url":"https://www.nhs.uk/conditions/prostate-cancer/help-and-support/"},{"label":"NHS: erection problems (erectile dysfunction)","url":"https://www.nhs.uk/conditions/erection-problems-erectile-dysfunction/"},{"label":"NHS: priapism (painful erections)","url":"https://www.nhs.uk/symptoms/priapism-painful-erections/"},{"label":"NHS: urinary incontinence","url":"https://www.nhs.uk/conditions/urinary-incontinence/"},{"label":"NHS: sepsis","url":"https://www.nhs.uk/conditions/sepsis/"},{"label":"NHS: clinical trials","url":"https://www.nhs.uk/tests-and-treatments/clinical-trials/"},{"label":"NHS: carer's assessments","url":"https://www.nhs.uk/social-care-and-support/support-and-benefits-for-carers/carer-assessments/"},{"label":"NHS: benefits for carers","url":"https://www.nhs.uk/social-care-and-support/support-and-benefits-for-carers/benefits-for-carers/"},{"label":"NICE NG234: spinal metastases and metastatic spinal cord compression, recommendations","url":"https://www.nice.org.uk/guidance/ng234/chapter/Recommendations"},{"label":"Prostate Cancer UK: just diagnosed","url":"https://prostatecanceruk.org/prostate-information-and-support/just-diagnosed"},{"label":"Prostate Cancer UK: localised prostate cancer","url":"https://prostatecanceruk.org/prostate-information-and-support/just-diagnosed/localised-prostate-cancer"},{"label":"Prostate Cancer UK: dealing with my diagnosis","url":"https://prostatecanceruk.org/prostate-information-and-support/just-diagnosed/dealing-with-my-diagnosis"},{"label":"Prostate Cancer UK: choosing a treatment","url":"https://prostatecanceruk.org/prostate-information-and-support/treatments/choosing-a-treatment"},{"label":"Prostate Cancer UK: follow-up after treatment","url":"https://prostatecanceruk.org/prostate-information-and-support/treatments/follow-up-after-treatment"},{"label":"Prostate Cancer UK: how hormone therapy affects you","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/how-hormone-therapy-affects-you"},{"label":"Prostate Cancer UK: hot flushes","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/how-hormone-therapy-affects-you/hot-flushes"},{"label":"Prostate Cancer UK: sex and relationships","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/sex-and-relationships"},{"label":"Prostate Cancer UK: treatments for erection problems","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/sex-and-relationships/treatments-for-erection-problems"},{"label":"Prostate Cancer UK: urinary problems after prostate cancer treatment","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/urinary-problems"},{"label":"Prostate Cancer UK: pelvic floor muscle exercises","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/pelvic-floor-muscle-exercises"},{"label":"Prostate Cancer UK: fatigue","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/fatigue"},{"label":"Prostate Cancer UK: the emotional impact","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/the-emotional-impact"},{"label":"Prostate Cancer UK: physical activity and prostate cancer","url":"https://prostatecanceruk.org/prostate-information-and-support/living-with-prostate-cancer/physical-activity-and-prostate-cancer"},{"label":"Prostate Cancer UK: metastatic spinal cord compression (MSCC)","url":"https://prostatecanceruk.org/prostate-information-and-support/advanced-prostate-cancer/metastatic-spinal-cord-compression-mscc"},{"label":"Prostate Cancer UK: our specialist nurses","url":"https://prostatecanceruk.org/prostate-information-and-support/get-support/our-specialist-nurses"},{"label":"Macmillan: prostate cancer","url":"https://www.macmillan.org.uk/cancer-information-and-support/prostate-cancer"},{"label":"Macmillan: hormonal therapies","url":"https://www.macmillan.org.uk/cancer-information-and-support/treatments-and-drugs/hormonal-therapies"},{"label":"Cancer Research UK: hormone therapy for prostate cancer","url":"https://www.cancerresearchuk.org/about-cancer/prostate-cancer/treatment/hormone-therapy"},{"label":"Royal Osteoporosis Society","url":"https://theros.org.uk/"},{"label":"Marie Curie: what is palliative care?","url":"https://www.mariecurie.org.uk/information/getting-care/palliative-care"},{"label":"Maggie's: support and information","url":"https://www.maggies.org/support-and-information/"},{"label":"Hamdy et al., fifteen-year outcomes after monitoring, surgery, or radiotherapy for prostate cancer (NEJM 2023)","url":"https://doi.org/10.1056/NEJMoa2214122"},{"label":"Donovan et al., patient-reported outcomes after monitoring, surgery, or radiotherapy for prostate cancer (NEJM 2016)","url":"https://doi.org/10.1056/NEJMoa1606221"},{"label":"Donovan et al., patient-reported outcomes 12 years after localized prostate cancer treatment (NEJM Evidence 2023)","url":"https://doi.org/10.1056/EVIDoa2300018"},{"label":"Shahinian et al., risk of fracture after androgen deprivation for prostate cancer (NEJM 2005)","url":"https://doi.org/10.1056/NEJMoa041943"},{"label":"Keating et al., diabetes and cardiovascular disease during androgen deprivation therapy for prostate cancer (JCO 2006)","url":"https://doi.org/10.1200/JCO.2006.06.2497"},{"label":"Shore et al., oral relugolix for androgen-deprivation therapy in advanced prostate cancer (HERO, NEJM 2020)","url":"https://doi.org/10.1056/NEJMoa2004325"},{"label":"Irani et al., venlafaxine, medroxyprogesterone acetate and cyproterone acetate for vasomotor hot flushes (Lancet Oncology 2010)","url":"https://doi.org/10.1016/S1470-2045(09)70338-9"},{"label":"Nead et al., androgen deprivation therapy and depression, systematic review and meta-analysis (Urologic Oncology 2017)","url":"https://doi.org/10.1016/j.urolonc.2017.07.016"},{"label":"UK National Screening Committee: prostate cancer recommendation","url":"https://view-health-screening-recommendations.service.gov.uk/prostate-cancer/"},{"label":"NICE NG131: prostate cancer, diagnosis and management","url":"https://www.nice.org.uk/guidance/ng131"},{"label":"National Prostate Cancer Audit: State of the Nation 2025","url":"https://www.natcan.org.uk/wp-content/uploads/2025/10/NPCA-SotN-2025.pdf"},{"label":"Prostate Cancer UK","url":"https://prostatecanceruk.org/"}],"tags":["gu","spike"],"related":["radiopharma-roadmap","psma-pet-to-rlt","beta-then-alpha","parp-plus-arpi","ai-pathology-to-adt","src-urotoday","prostate-ductal-adenocarcinoma","prostate-nepc","prostate-low-risk","prostate-intermediate-risk","prostate-high-risk","prostate-bcr","prostate-mhspc","prostate-nmcrpc","prostate-mcrpc","prostate-roadmap","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-bipolar-androgen-therapy-phase-3-on-pfs2","idea-prostate-metastatic-presentation-as-the-screening-endpoint","idea-prostate-other-cause-mortality-as-a-reported-service-outcome","idea-prostate-per-lesion-mri-audit-before-focal-treatment","ar-amplification","ar-ligand-binding-domain-mutation","ar-v7-splice-variant","hrr-gene-mutation","tmprss2-erg-fusion","spop-mutation","nepc-transformation","ctdna-tumour-fraction","psma-pet-expression","brca-germline","brca-somatic","pten-alteration","msi-high","dmmr-ihc","hrd-positive","tmb-high"],"cancers":[],"sections":[],"technologies":["psma-pet","radioligand-therapy","targeted-alpha-therapy","androgen-deprivation","parp-inhibitor","digital-pathology-ai","robotic-surgery","brachytherapy","hifu-histotripsy","hyperbaric-oxygen-radiation-injury","active-surveillance","mp-mri","t-cell-engager","epigenetic-drugs","germline-testing","cytotoxic-chemotherapy","palliative-care","palliative-radiotherapy","psycho-oncology","peer-support-groups","oncology-nutrition","pain-management","survivorship-care-plan","multidisciplinary-tumour-board","financial-navigation","cbt-fatigue-distress","exercise-during-chemotherapy","prehabilitation","prostate-screening-psa-mri","mri","pet","checkpoint-inhibitor","liquid-biopsy","wes-wgs","sbrt","cgp","histopathology-ihc","cytogenetics-fish","rna-seq","methylation-profiling","pet-ct"],"targets":["psma","androgen-receptor","parp","brca","akt","b7h3","dll3","steap1","klk2","grpr","ezh2","atm","cdk12","tp53","rb1","pten","erg","tmprss2","foxa1","spop","pik3ca","etv1","palb2","msh2","nkx3-1","apc","kmt2c","zbtb16","idh","aurka","cdkn1b"],"drugs":["paige-prostate","mitoxantrone","nilutamide","triptorelin","prednisone","padeliporfin","samarium-153-lexidronam","abiraterone","enzalutamide","apalutamide","darolutamide","docetaxel","cabazitaxel","estramustine","olaparib","rucaparib","niraparib","talazoparib","pluvicto","radium-223","sipuleucel-t","pembrolizumab","capivasertib","leuprolide","bicalutamide","zoledronic-acid","carboplatin"],"companies":["halda-therapeutics","orion-orion-pharma","shenzhen-ionova-life-sciences","futurechem","hinova-pharmaceuticals","mbrace-therapeutics","spectracure","novartis","bayer","pfizer","astellas","johnson-johnson","astrazeneca","amgen","lantheus","telix","curium","veracyte","artera"],"institutions":["royal-marsden","icr-london","peter-mac","ucla-jonsson","uke-hamburg","johns-hopkins","gustave-roussy","prostate-cancer-uk","uclh","leeds-cancer-centre","the-christie","clatterbridge","imperial-cancer-centre","velindre-cardiff","beatson-glasgow","northern-ireland-cancer-centre"],"pathways":["ar-signaling","pi3k-akt-mtor","ddr","prostate-cancer-signalling","homologous-recombination-repair","base-excision-repair-parp","synthetic-lethality-map","lineage-plasticity-neuroendocrine","p53-cell-cycle","mismatch-repair-msi","wnt","ubiquitin-proteasome-system","epigenetic-reprogramming","chromosomal-instability","clonal-evolution","intravasation-ctc-survival"],"terms":["psa","gleason-grade-group","castration-resistance","biochemical-recurrence","psa50","ar-v7","theranostics","oligometastatic","crossover","cambridge-prognostic-group","tnm-prostate-cancer","prostate-acinar-adenocarcinoma","intraductal-carcinoma-prostate","cribriform-prostate-cancer","percentage-gleason-pattern-4","psa-density","extraprostatic-extension","high-grade-pin","watchful-waiting","mcrpc-mhspc","psa-kinetics","active-surveillance-term","tnm-staging","grade-vs-stage","tumour-grade","prostatectomy","orchiectomy","bone-metastases","cancer-related-fatigue","curative-intent","late-effects","performance-status","quality-of-life","febrile-neutropenia","overdiagnosis","adt","hrd","msi","tmb","ctdna","ngs","ihc","screening","synthetic-lethality","hazard-ratio","radiotherapy","prostate-treatment-choice-localised","prostate-radiotherapy-fractionation","prostate-stampede-arms","prostate-adt-burden","prostate-crpc-sequencing","prostate-hrr-eligibility","prostate-failed-programmes","prostate-uk-drug-approvals","prostate-focal-therapy","lead-time-bias","overtreatment","number-needed-to-screen","other-cause-mortality","metastasis-free-survival","radiographic-progression-free-survival","chromoplexy","genome-wide-loss-of-heterozygosity","polygenic-risk-score","neuroendocrine-differentiation","whole-mount-pathology","pi-rads","template-mapping-biopsy","bipolar-androgen-therapy","intermittent-androgen-deprivation","germline-vs-somatic","gbrca-mutation","brca-reversion-mutations","lynch-syndrome","histologic-transformation","cfdna","liquid-biopsy","biopsy","gene-fusion","gene-amplification","amplification","copy-number-variation-term","driver-mutation","resistance","cross-resistance","vus","somatic-mutations-wxs-wgs","fish","tumour-agnostic"],"trials":["nct06136624","nct06136650","nct06952803","nct06120491","nct06855277","nct06780670","nct07365995","nct06764485","mcrpc","himalayas-1","nct07311694","nct07615101","nct07649122","nct05381103","rtog-9601","horrad","pop-rt","nct06629779","nct05348577","nct05939414","nct06520345","nct07028853","nct01436968","nct03706365","nct04076059","nct05884398","nct07213674","nct04446117","nct06925737","nct07052214","nct05171816","nct07611110","nct04691804","nct05794906","nct02489318","nct04557059","nct03348670","nct06235151","nct02257736","nct06754085","nct06970847","nct04821622","nct05288166","nct07225946","nct04497844","nct03767244","nct02531516","nct01946204","nct06056830","nct03851640","stampede","protect","chaarted","latitude","vision","profound","propel","talapro-2","magnitude","embark","arasens","peace-1","enzamet","prosper","aramis","alsympca","psmaddition","capitello-281","goteborg-2","promis","transform-prostate","chhip","pace-b"],"people":["chris-hoy","jenny-donovan","caroline-moore","nicholas-van-as","ros-eeles","rakesh-heer"],"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","b-undruggable-targets","b-tumor-heterogeneity","b-generic-repurposing","b-aging-comorbidity"],"keyPapers":["paper-taplin-ar-mutation-androgen-independent-prostate-nejm-1995","paper-quigley-structural-variation-mcrpc-cell-2018","paper-prophecy-arv7-validation-jco-2019","paper-scher-nuclear-arv7-taxane-vs-arsi-jama-oncol-2018","paper-barbieri-spop-foxa1-med12-prostate-nat-genet-2012","paper-abida-genomic-correlates-outcome-mcrpc-pnas-2019","paper-armenia-long-tail-oncogenic-drivers-prostate-nat-genet-2018","paper-kumar-interindividual-genomic-diversity-metastatic-prostate-nat-med-2016","paper-stopsack-mcspc-genomic-alterations-outcomes-ccr-2020","paper-stopsack-prostate-genomes-by-race-ccr-2022","paper-ren-chinese-prostate-whole-genome-eur-urol-2018","paper-mateo-genomics-lethal-prostate-diagnosis-castration-resistance-jci-2020","paper-nicolosi-germline-variants-prostate-testing-guidelines-jama-oncol-2019","paper-castro-germline-brca-prostate-outcomes-jco-2013","paper-isaacsson-velho-intraductal-germline-dna-repair-prostate-2018","paper-taylor-germline-brca2-evolutionary-trajectories-nat-commun-2017","paper-quigley-brca2-reversion-cfdna-parp-resistance-cancer-discov-2017","paper-jensen-clonal-haematopoiesis-cfdna-interference-prostate-jama-oncol-2021","paper-carver-pi3k-ar-reciprocal-feedback-prostate-cancer-cell-2011","paper-ferraldeschi-pten-protein-loss-abiraterone-eur-urol-2015","paper-ipatential150-ipatasertib-abiraterone-pten-lancet-2021","paper-pettersson-tmprss2-erg-outcome-meta-analysis-cebp-2012","paper-abida-msi-prostate-checkpoint-blockade-jama-oncol-2019","paper-pritchard-complex-msh2-msh6-hypermutated-prostate-nat-commun-2014","paper-guedes-msh2-loss-primary-prostate-ccr-2017","paper-silver-psma-expression-normal-malignant-tissues-ccr-1997","paper-fendler-psma-pet-biochemical-recurrence-jama-oncol-2019","paper-epstein-neuroendocrine-prostate-morphologic-classification-ajsp-2014","paper-beltran-nepc-aurka-mycn-cancer-discov-2011","paper-ku-rb1-trp53-lineage-plasticity-science-2017","paper-bluemn-double-negative-prostate-fgf-mapk-cancer-cell-2017","paper-labrecque-mcrpc-phenotypes-jci-2019","paper-aparicio-aggressive-variant-prostate-tumour-suppressors-ccr-2016","paper-berchuck-cfdna-methylation-nepc-detection-ccr-2022","paper-wyatt-ctdna-tissue-concordance-mcrpc-jnci-2017","paper-annala-ctdna-resistance-abiraterone-enzalutamide-cancer-discov-2018","paper-tukachinsky-ctdna-3334-advanced-prostate-ccr-2021","paper-beltran-nepc-divergent-evolution-nat-med-2016","paper-propsma-hofman-lancet-2020","paper-therap-lancet-2021","paper-profound-nejm-2020","paper-vision-nejm-2021","paper-visakorpi-androgen-receptor-amplification-nat-genet-1995","paper-chen-androgen-receptor-overexpression-antiandrogen-resistance-nat-med-2004","paper-antonarakis-ar-v7-resistance-nejm-2014","paper-tcga-molecular-taxonomy-primary-prostate-cell-2015","paper-grasso-mutational-landscape-lethal-crpc-nature-2012","paper-taylor-integrative-genomic-profiling-cancer-cell-2010","paper-robinson-integrative-clinical-genomics-advanced-prostate-cell-2015","paper-pritchard-inherited-dna-repair-metastatic-prostate-nejm-2016","paper-tomlins-tmprss2-ets-fusion-science-2005","paper-abida-triton2-rucaparib-brca-jco-2020","paper-mu-sox2-lineage-plasticity-science-2017"],"journals":["clinical-genitourinary-cancer","prostate-cancer-and-prostatic-diseases","urologic-oncology"],"dependsOn":[],"notes":["Which page is mine? Prostate cancer is described by five things at once, and each has its own page here. The type is almost always acinar adenocarcinoma, which is this page; if the report says ductal, or says the cancer turned neuroendocrine after hormone treatment, there is a page for each. The grade is a grade group from 1 to 5 with a Gleason score beside it. The stage is a TNM category. The risk band in Britain is a Cambridge Prognostic Group from 1 to 5, and the localised pages here are mapped to it: CPG 1 is the low-risk page, CPG 2 and 3 the intermediate-risk page, CPG 4 and 5 the high-risk page. The state is whether the cancer still responds to hormone treatment and whether it has spread, and there are pages for rising PSA after treatment, for metastatic hormone-sensitive disease, for non-metastatic and metastatic castration-resistant disease.","What prostate cancer is. The prostate is a gland the size of a walnut that sits below the bladder and surrounds the top of the urethra, and it makes the fluid that carries sperm. More than 95 in every 100 prostate cancers arise in its acini, the small glands that make that fluid, which is why the ordinary type is called acinar adenocarcinoma. It usually starts on the outer part of the gland, which is why it usually causes nothing at first, and why so much of it is found by a blood test rather than by a symptom.","Why the same cancer gets different risk labels on either side of the Atlantic. Britain and America stratify localised prostate cancer with different systems. NICE NG131 recommendation 1.2.15 uses the five Cambridge Prognostic Groups; the NCCN uses six bands, from very low to very high, and splits intermediate risk into favourable and unfavourable using criteria the Cambridge system does not have, including PSA density and the proportion of positive cores. NICE replaced its own three-tier table, which came from D'Amico, in the 2021 amendment because the three-tier model could not tell Gleason 3+4 from 4+3, and the Cambridge system can. A man reading an American source about his own diagnosis is reading a different map of the same ground.","Is the Gleason score being replaced by the grade group? No. They are used together, and a UK report in 2026 gives both. The Royal College of Pathologists dataset sets out the grade groups to be used 'in tangent with the Gleason score', and its proforma asks for each separately. The grade groups exist to split Gleason 7, which is really two diseases, 3+4 and 4+3, into grade groups 2 and 3. NICE's Cambridge table is written with both scales in every row for the same reason: the Gleason score is what appears in older notes and in most of the literature.","Why does my report mention cribriform or intraductal when my grade is only 7? Because since October 2024 the UK reporting dataset asks for it, and because within grade group 2 and 3 those patterns are where the risk sits. Invasive cribriform carcinoma is the worst-behaving form of Gleason pattern 4, and intraductal carcinoma is cancer filling ducts that still have their outer basal layer. Either one argues against active surveillance, and either one is a reason to be offered germline genetic testing under both the NCCN and the Philadelphia consensus recommendations.","Grade group 1 prostate cancer and the word cancer. Grade group 1, Gleason 6, is the grade that has prompted a long argument about whether it should be called cancer at all, because left alone it very rarely spreads. NICE's answer is practical rather than semantic: Cambridge Prognostic Group 1, which is grade group 1 with a PSA under 10 and stage T1 or T2, is the one band where active surveillance is offered first and radical treatment is a fallback if surveillance is unsuitable or unacceptable to the person (NG131 1.3.8).","Am I being watched, or watched and left? Active surveillance and watchful waiting are different plans with different intentions. Active surveillance monitors with PSA, repeat MRI and repeat biopsy so that a cancer that changes can still be cured. Watchful waiting, in NICE's own definition, is a strategy for controlling rather than curing, for people who do not want radical treatment or for whom it is not suitable, and relies on deferred hormone therapy. Both involve not treating today; only one keeps cure on the table.","How common is it, and what is the outlook? Worldwide, 1,546,112 new cases and 419,849 deaths a year, fourth for cases among all cancers and eighth for deaths (GLOBOCAN 2024). In the UK, 57,898 new cases and 12,300 deaths a year, and 78.9 percent of men survive ten years or more; the lifetime risk of being diagnosed is 17 percent (Cancer Research UK). In the United States 333,830 cases and 36,320 deaths are projected for 2026, and 69.5 percent are found while still confined to the prostate, where five-year relative survival is 100 percent (SEER). These are averages over everybody diagnosed and they are not a personal prognosis; for most men the question the numbers raise is not whether treatment will work but whether treatment is needed at all.","Why the histology tier here is short. The WHO fifth edition names ductal adenocarcinoma, treatment-related neuroendocrine prostatic carcinoma, adenoid cystic (basal cell) carcinoma, and squamous and adenosquamous carcinoma as types separate from acinar adenocarcinoma, and lists PIN-like carcinoma as a subtype of acinar adenocarcinoma with the atrophic, pseudohyperplastic, microcystic and foamy-gland appearances as patterns rather than entities. The first two have pages here because they change management; the rest are rare enough that the honest treatment is a sentence on this page and a glossary entry, not a thin page of their own. Urothelial carcinoma of the prostatic urethra is covered in the urinary tract chapter of the same classification, so it is not a prostate cancer record here.","Living with prostate cancer, care and decisions: This is orientation from public patient pages and guidelines, not advice for your case: your own team's instructions and 24-hour number come first. The eight decision rows on this page, the question sets for the urology, surgical, oncology, hormone therapy, sexual function and continence and palliative care appointments and for partners and carers, the first 60 days checklist and the red cards were written from NICE NG131 and NG234 and from the NHS, Prostate Cancer UK, Macmillan, Cancer Research UK, Marie Curie and Maggie's, with the patient-reported figures taken from the ProtecT trial's own publications rather than from summaries of them.","On the numbers in these rows. They come from ProtecT, a UK trial that randomly assigned 1,643 men aged 50 to 69 with PSA-detected, mostly Cambridge Prognostic Group 1 to 3 disease to active monitoring, prostatectomy or radiotherapy, and followed them for a median of 15 years with questionnaire response rates above 80 percent. They describe what happened to that group. They are not a forecast for one man, and no sentence here should be read as one. Where NICE has put the same figures into its own box 2, the guideline's wording is used, because that is the table a clinician is meant to work through with you.","On plain words. These pages call incontinence leaking and calls impotence not being able to get an erection, and gives both their numbers. Men do not raise either subject, surveys consistently find they are not asked about them either, and the result is that the commonest long-term consequences of treating this cancer arrive unannounced. NICE NG131 (1.1.12) requires that sexual function, physical appearance, continence and other aspects of masculinity are discussed before treatment. Nothing here assumes the reader is old, uninterested in sex, or has a partner.","On hormone therapy. It is the longest-running part of this illness for most men who need it and the least covered anywhere. The row on living with hormone therapy collects what NICE offers for each effect, because almost every one of them has an answer: medroxyprogesterone for hot flushes, a fracture risk assessment and bone drugs where osteoporosis is present, six-monthly metabolic checks, supervised resistance and aerobic exercise twice a week for 12 weeks for fatigue, prophylactic breast bud radiotherapy for men on long-term bicalutamide, psychosexual counselling for couples, and intermittent therapy where the setting allows it.","The words that carry the screening argument, in one place. Lead time is how much earlier a screening test found the cancer, and lead-time bias is the mistake of counting that extra knowing as extra life; overdiagnosis is a lead time longer than the rest of the man's life; overtreatment is the harm that follows when an overdiagnosed cancer is treated. The number needed to screen turns all of it into one figure a health service can weigh: at 16 years in the European randomised trial, 570 men invited and 18 extra cancers diagnosed to prevent one prostate cancer death.","Two words for the same scan, and they are not the same score. The international system is PI-RADS, now version 2.1, which builds a 1 to 5 assessment category from fixed per-sequence rules. NICE NG131 1.2.2 asks United Kingdom reports to use a 5-point Likert scale instead, which is the radiologist's overall probability judgement using the clinical picture as well as the images. Both run 1 to 5 and both trigger a biopsy at 3 or more, and a man reading an American source about his own scan is reading a different scale.","The science in detail, 1 of 7, in full; the one-sentence version is on the overview. The androgen receptor, five routes to the same place. Amplification of the gene at Xq12: 48.9% of 444 samples in prad_su2c_2019, 52.0% of 150 in prad_su2c_2015 and 57.0% of 149 in prad_fhcrc, against 1.0% of 489 TCGA primaries and 4.0% of 424 metastatic castration-sensitive samples, first shown as a treatment effect in 7 of 23 recurrent tumours with none in the matched pre-treatment specimens. Amplification of an intergenic enhancer 624 kb upstream, in 81% of 101 deeply sequenced metastases, invisible to coding-exon panels. Ligand-binding-domain mutation in 13.7 to 18.0% of castration-resistant cohorts against 0.4% of primaries, clustered on four residues: L702H, which makes the receptor responsive to glucocorticoid; T878A and H875Y, which open it to progestogens; and F877L, which turns enzalutamide and apalutamide into agonists. The AR-V7 splice variant, which deletes the drug-binding domain altogether, detectable in circulating tumour cells from 39% of men starting enzalutamide and 19% starting abiraterone. And simply raising receptor expression, which was shown in xenografts to be necessary and sufficient for resistance on its own. In plasma, some potential androgen receptor resistance alteration is present in 42% of 2,213 evaluable men, often polyclonal or compound.","The science in detail, 2 of 7, in full; the one-sentence version is on the overview. The landscape by stage. Localised disease, from the TCGA primary cohorts: ERG fusion 45.6% of 333, ETV1 8.7%, ETV4 4.8%, FLI1 1.2%; SPOP mutation 11.1%; FOXA1 mutation 5.7%; PTEN deep deletion 17.4%; TP53 mutation 11.5%, falling to 3.4% in the CPC-GENE localised whole genomes; NKX3-1 deletion 8.0 to 15.9%; CHD1 deletion 7.0%; MYC amplification 8.2%; RB1 deletion 9.4%; BRCA2 mutation 1.6% with deletion 3.5%; ATM mutation 4.0%; CDK12 mutation 1.8%. Metastatic castration-resistant disease, from prad_su2c_2019 and its companions: TP53 36.7%, PTEN deletion 25.7%, AR amplification 48.9%, MYC amplification 23.6%, RB1 deletion 9.7%, BRCA2 mutation 8.3%, ATM 6.1%, CDK12 5.9%, SPOP falling to 5.6%. Metastatic castration-sensitive disease sits between, from 424 men: TP53 30.4%, PTEN deletion 14.4%, AR amplification 4.0%, SPOP 12.5%. Ancestry adds a third axis: in 65 Chinese tumours, CHD1 deletion reaches 20.0% while ERG rearrangement is 6.2%, and in 2,069 men at one centre, tumours from Black men carried more AR alterations, fewer PTEN mutations and more 8q gain, and tumours from Asian men more FOXA1 and ZFHX3 alterations.","The science in detail, 3 of 7, in full; the one-sentence version is on the overview. DNA repair, germline against somatic. Inherited mutations in 20 repair genes were present in 82 of 692 men with metastatic prostate cancer unselected for family history, 11.8%: BRCA2 5.3%, ATM 1.6%, CHEK2 1.9%, BRCA1 0.9%, RAD51D 0.4% and PALB2 0.4%, against 4.6% in localised disease and 2.7% in a 53,105-person reference population, with no difference by family history or age at diagnosis. On a broader panel in 3,607 men, 17.2% had a positive result and only 30.7% of those were BRCA, with mismatch repair variants in 1.74% of all men tested and 37% of positives ineligible for testing under the guideline then in force. Somatically, BRCA2, BRCA1 and ATM aberrations together were 19.3% of 150 metastatic castration-resistant tumours. A tumour report cannot answer the germline question and a separate consented test is needed; a plasma report cannot answer it either, and in 10% of men an ATM, BRCA2 or CHEK2 variant in plasma has come from the bone marrow rather than the prostate, which a paired whole-blood control distinguishes. Pathology gives a hint: intraductal or ductal histology was present in 48% of germline carriers against 12% of non-carriers in one 150-man series, and localised tumours from germline BRCA2 carriers already look metastatic in their genomes.","The science in detail, 4 of 7, in full; the one-sentence version is on the overview. The four PARP inhibitor eligibility lists, read from the labels. Olaparib alone after enzalutamide or abiraterone: 14 genes, ATM, BRCA1, BRCA2, BARD1, BRIP1, CDK12, CHEK1, CHEK2, FANCL, PALB2, RAD51B, RAD51C, RAD51D and RAD54L, germline or somatic. Olaparib with abiraterone: BRCA1 and BRCA2 only. Rucaparib after androgen receptor-directed therapy: BRCA1 and BRCA2 only, germline and/or somatic. Niraparib with abiraterone: BRCA2 alone in castration-sensitive disease and BRCA1 or BRCA2 in castration-resistant disease. Talazoparib with enzalutamide: 12 genes, ATM, ATR, BRCA1, BRCA2, CDK12, CHEK2, FANCA, MLH1, MRE11A, NBN, PALB2 and RAD51C, of which ATR, FANCA, MLH1, MRE11A and NBN are not on olaparib's list and seven of olaparib's genes are not on this one, with the label stating that no approved test for them exists. The response data behind the widest list: among men with a single-gene alteration and measurable disease in PROfound, confirmed objective response was 24 of 43 with BRCA2, 56%, 3 of 30 with ATM, 10%, and 2 of 34 with CDK12, 6%, with none among the eleven rarer genes, one or two men each. PPP2R2A was enrolled and then left out of the indication for unfavourable benefit and risk.","The science in detail, 5 of 7, in full; the one-sentence version is on the overview. PSMA, an imaging target and a therapeutic one. The tissue survey behind it found PSMA detectable in prostatic epithelium, duodenal mucosa, a subset of proximal renal tubules and colonic neuroendocrine cells and in no other normal tissue, staining 33 of 35 primary prostate adenocarcinomas and 7 of 8 nodal metastases but only 8 of 18 bone metastases, with expression falling as tumours dedifferentiate. At staging, PSMA PET-CT was 27% more accurate than CT with bone scan in 302 randomised men, 92% against 65%, with sensitivity 85% against 38% and specificity 98% against 91%, management change in 28% against 15%, equivocal findings in 7% against 23%, and radiation of 8.4 against 19.2 mSv. At biochemical recurrence it localised disease in 475 of 635 men, 75%, with detection rates of 38% below PSA 0.5 ng/mL, 57% at 0.5 to 1.0, 84% at 1.0 to 2.0, 86% at 2.0 to 5.0 and 97% above 5.0, and positive predictive value 0.84 by histopathology. For radioligand therapy the criterion is lesion by lesion: at least one lesion with uptake greater than normal liver, and no lesion above a size threshold with uptake at or below liver. Of 291 men screened for TheraP, 200, 69%, were eligible. What the scan cannot do is give a histology or a genotype, and a PSMA-low, FDG-avid site in a man on hormonal treatment is one of the ways lineage change announces itself.","The science in detail, 6 of 7, in full; the one-sentence version is on the overview. Leaving the androgen receptor behind. The transition is epigenetic before it is genetic: whole-exome sequencing showed substantial genomic overlap between castration-resistant adenocarcinoma and neuroendocrine disease from the same men, fitting divergent clonal evolution, while methylation separated the two sharply and reassigned some tumours that looked like adenocarcinoma. The genotype that permits it is loss of both RB1 and TP53, shown in mouse models where Rb1 loss enabled lineage plasticity and metastasis and additional Trp53 loss caused antiandrogen resistance, with Ezh2 and Sox2 raised and EZH2 inhibition restoring receptor expression, and in human cells where the shift from luminal to basal-like identity required TP53 and RB1 loss and was mediated by SOX2. Combined RB1, TP53 and PTEN alterations were enriched in clinically defined aggressive variant disease, with RB1 copy loss the strongest single discriminator at 54% of 44 samples. Neuroendocrine is not the only exit: an androgen receptor-null, neuroendocrine-null phenotype sustained by FGF and MAPK signalling has emerged over two decades, and deep phenotyping resolves five states rather than two. Recognition is morphological first, using the six named categories, with AURKA and MYCN co-amplification in 40% of neuroendocrine tumours against 5% of adenocarcinomas, and cell-free DNA methylation discriminated the two states with an area under the curve of 0.96 and 1.0 in two cohorts totalling 101 men.","The science in detail, 7 of 7, in full; the one-sentence version is on the overview. Liquid biopsy, and why it matters more here. Prostate cancer metastasises to bone, and bone is the hardest tissue to biopsy well, so plasma is not a convenience here but often the only practical sample. Above a 2% tumour fraction, which 75.6% of paired samples reached, every somatic mutation found in a matched metastatic biopsy was also present in plasma, with copy-number calls in actionable genes 88.9% concordant. At scale, 94% of 3,334 men had detectable circulating tumour DNA at a median fraction of 7.5%, and 93% of tissue-detected BRCA mutations were found in plasma including 100% of predicted germline variants. Plasma sees more than tissue where it counts: potential androgen receptor resistance alterations in 42% of 2,213 men, including polyclonal and compound mutations and exon 8 deletions, and multiclonal BRCA2 reversions at PARP inhibitor resistance. It cannot separate germline from somatic without a consented germline test, cannot give a histology, cannot measure PSMA, and cannot by itself distinguish a repair-gene variant from the tumour from one from the bone marrow: at a 2% threshold, 19% of men had clonal haematopoiesis variants in plasma and 10% had one in a gene used to decide PARP inhibitor candidacy, most often ATM, accounting for almost half of all somatic repair-gene variants detected. A paired whole-blood control fixes it. Before treatment starts, the useful plasma signal is in BRCA2, ATM and TP53 rather than in the AR amplification that dominates the report.","Frequencies marked cBioPortal were computed from the public API on 25 September 2026 on the deposited sample lists of prad_tcga_pan_can_atlas_2018 (494 sequenced, 489 with copy number, 494 with structural variants), prad_tcga_pub (333), prad_broad (112), prad_cpcg_2017 (477, mutations only), prostate_dkfz_2018 (313, mutations only), prad_eururol_2017 (65), prad_p1000 (1,013), prad_mskcc_2017 (504), prostate_msk_2024 (2,260), prad_msk_stopsack_2021 (2,069), prad_cdk12_mskcc_2020 (1,465), prad_mcspc_mskcc_2020 (424), prad_su2c_2019 (444), prad_su2c_2015 (150), prad_mich (61), prad_fhcrc (141 sequenced, 149 with copy number), nepc_wcm_2016 (114, mutations only) and mpcproject_broad_2021 (82), as sample-level counts of non-synonymous mutation, high-level amplification, deep deletion or structural variant. They are not the papers' own percentages, which are quoted alongside where the abstract gives them.","What the deposits cannot see, stated once so the rows do not have to repeat it. Fusion counts come from the structural-variant profile, so a cohort with no such profile reads zero rather than negative for TMPRSS2-ERG, and a targeted DNA panel that does not bait the breakpoint introns reads about 25% where whole-exome and RNA cohorts read 41 to 46%. The metastatic whole-exome deposits call high-level amplification on chromosome arms gained as a block, so genes near a real amplicon read high: NBN at 8q21 reads 20.5% in prad_su2c_2019 next to MYC at 8q24, and BRIP1, RAD51C, ATR and PMS2 read similarly inflated there, which is why only AR, MYC and the ETS loci are quoted as focal from those deposits. The CPC-GENE and DKFZ localised deposits carry mutation calls only, so their low TP53 and PTEN figures are partly a property of the deposit. Panel cohorts mix primary and metastatic samples, so their figures sit between the two stages rather than describing either."],"group":"genitourinary","burden":"~1.5 million new cases per year worldwide; lifetime risk ~1 in 8 men in high-income countries; median age at diagnosis 67; most PSA-detected disease is indolent and safely watched. ~400,000 deaths per year worldwide, mostly from disease that was already metastatic at diagnosis.","subtypes":["Localised: low / favourable-intermediate / unfavourable-intermediate / high risk (NCCN)","Non-metastatic castration-resistant (nmCRPC)","Metastatic hormone-sensitive (mHSPC; FDA 2026 term 'androgen pathway modulation-naive or -sensitive'), de novo vs recurrent, high vs low volume (CHAARTED)","Metastatic castration-resistant (mCRPC)","HRR-mutant (~20-25% of mCRPC; BRCA2 most actionable)","PTEN-deficient (~25% on CAPItello-281's immunohistochemistry cut-off, 47% on IPATential150's)","PSMA-low / heterogeneous (about a tenth screened out on VISION's criteria, 31% on TheraP's)","Treatment-emergent neuroendocrine prostate cancer (10.5 to 17% of late mCRPC)","Ductal and intraductal / cribriform variants (aggressive)","Prostatic ductal adenocarcinoma","Rare histologies, treated as they are named by the WHO fifth edition: adenoid cystic (basal cell) carcinoma, squamous and adenosquamous carcinoma, prostatic stromal sarcoma","Cambridge Prognostic Group 1 to 5, the five-band NHS risk stratification of localised and locally advanced disease (NICE NG131 1.2.15)"],"biomarkers":["PSA","Gleason / Grade Group","PSMA PET","HRR genes (BRCA2, ATM, etc.)","PTEN","MSI","AR-V7 (research)","Decipher / ArteraAI","PSA, PSA density, PSA doubling time","Grade Group (Gleason) and cribriform/intraductal pattern","mpMRI PI-RADS score","PSMA PET (SUVmax, total tumour volume) for staging and radioligand eligibility","Germline and somatic HRR genes (BRCA2, BRCA1, ATM, PALB2, CDK12)","PTEN loss (IHC or NGS) for capivasertib","MSI/dMMR (~3%, pembrolizumab)","Decipher genomic classifier; ArteraAI digital pathology","AR-V7 (CTC) in research/limited use","Testosterone level (castration confirmation)","Neuroendocrine markers (chromogranin, synaptophysin, RB1/TP53 loss) on progression","Grade group and Gleason score together, as UK reports give both (RCPath G084, October 2024)","Percentage of Gleason pattern 4, a core reporting item in core biopsies since the 2024 UK dataset","Presence of intraductal carcinoma or invasive cribriform carcinoma, a core reporting item and a trigger for germline testing","PSA density, the PSA divided by the MRI prostate volume, used in the very-low-risk definition and in deciding against biopsy","Cambridge Prognostic Group 1 to 5, assigned by the MDT to every newly diagnosed localised or locally advanced case (NICE NG131 1.2.15)","TMPRSS2-ERG: 25-46%","SPOP: 6-14%","FOXA1: 2-16%","PTEN: 12-41%","TP53: 3-41%","AR: 1-57%","AR ligand-binding-domain mutation: 0.4-18%","RB1: 3-23%","BRCA2: 3-11%","ATM: 3-11%","CDK12: 1-6%","BRCA1: 0.2-2%","Mismatch repair genes: 0.2-3%","Microsatellite instability: 3.1%","PSMA (FOLH1): 80-95%"],"standardOfCare":[{"setting":"Screening","approach":"Shared-decision PSA testing from 50 (45 if Black or family history/BRCA), risk-adapted intervals; MRI before biopsy; avoid biopsy if MRI negative and PSA density low.","refs":["psa","mp-mri","precision-mri","germline-testing","erspc","plco-prostate"]},{"setting":"Biochemical recurrence","approach":"PSMA PET to localise; salvage radiotherapy ± ADT after prostatectomy; metastasis-directed SBRT for oligorecurrence (investigational for survival); enzalutamide ± ADT for high-risk BCR (EMBARK).","refs":["psma-pet","biochemical-recurrence","embark","enzalutamide","sbrt","idea-psma-pet-guided-mdt"]},{"setting":"Metastatic hormone-relapsed disease: what is in trials once the approved order runs out","approach":"The approved sequence is in the hormone-relapsed row above. After it, the options are trials: actinium-225 PSMA radioligand therapy for men who have progressed on lutetium-177 (AlphaBreak), the STEAP1 T-cell engager xaluritamig (XALUTE) and the KLK2 engager pasritamig, the EZH2 inhibitor mevrometostat with enzalutamide (MEVPRO-1), and, for treatment-emergent neuroendocrine disease, platinum with etoposide outside a trial and the DLL3 and B7-H3 agents borrowed from small cell lung cancer, tarlatamab and ifinatamab deruxtecan.","refs":["ac225-psma","alphabreak","xaluritamig","xalute","pasritamig","mevrometostat","mevpro-1","tarlatamab","ifinatamab-deruxtecan"]},{"setting":"Localised prostate cancer: monitoring, surgery or radiotherapy, and what each one costs you","approach":"This is the decision the whole of prostate cancer turns on, and it is unusual because the three options are not ranked. NICE NG131 (1.3.8 to 1.3.12) writes one recommendation per Cambridge Prognostic Group: active surveillance is offered first at CPG 1, a choice between all three is offered at CPG 2, radical treatment is offered at CPG 3 with surveillance kept open for men who choose not to be treated immediately, and surveillance is not offered at CPG 4 and 5. If you were given a risk band instead of a number, the bridge is that CPG 1 is low risk, CPG 2 and 3 are intermediate risk and CPG 4 and 5 are high risk; the group is worked out from your Gleason score or grade group, your PSA and your T stage, and a UK pathology report carries the Gleason score and the grade group together. For CPG 1 to 3, NICE (1.3.7) sends the conversation to its box 2, which is a table of what happened to 100 men offered each option in the UK ProtecT trial, and the honest summary of that table is that survival was the same and the harms were not. On survival, box 2 reports that at 10 years, 98 out of 100 men offered monitoring, 99 out of 100 offered prostatectomy and 99 out of 100 offered radiotherapy had not died of prostate cancer, and that the evidence does not show a difference between them. At a median of 15 years the trial found death from prostate cancer in 17 of 545 men (3.1 percent) on monitoring, 12 of 553 (2.2 percent) after prostatectomy and 16 of 545 (2.9 percent) after radiotherapy, with the overall comparison not significant. What treatment changed was spread: metastases in 51 men (9.4 percent) on monitoring against 26 (4.7 percent) and 27 (5.0 percent), and clinical progression in 141 (25.9 percent) against 58 (10.5 percent) and 60 (11.0 percent). A quarter of the monitoring group, 133 men, were alive at the end of follow-up with no prostate cancer treatment of any kind. On continence, box 2 reports moderate to severe incontinence at 6 months in 19 out of 100 men offered prostatectomy against 4 on monitoring and 6 after radiotherapy, and at 6 years in 13, 8 and 5. The trial's own patient-reported figures are blunter: pad use went from 1 percent before treatment to 46 percent at 6 months after surgery, against 4 percent and 5 percent in the other two groups, and was still 17 percent at 6 years and 18 to 24 percent through years 7 to 12. On sexual function, box 2 reports moderate or severe erectile dysfunction at 6 months in 66 out of 100 men offered prostatectomy, 48 after radiotherapy and 29 on monitoring, and at 6 years in 50, 36 and 40. Of the men in the trial, 67 percent could get an erection firm enough for intercourse before anything was done; at 6 months that was 12 percent after surgery, 22 percent after radiotherapy and 52 percent on monitoring, and by year 12 all three groups had converged at a low level. On bowels, radiotherapy is the one that costs: moderate to severe impact of bowel habits on quality of life at 6 months in 10 out of 100 men offered radiotherapy against 3 in each other group, and faecal leakage in 12 percent of the radiotherapy group against 6 percent of the others by year 12. Nothing in this row is a prediction about one man. It is what happened to 1,643 UK men aged 50 to 69 with mostly CPG 1 to 3 disease, and the reason to read it is that it names the trade-off rather than gesturing at it. NICE surrounds the choice with process: a decision aid in the clinic (1.1.6), nomograms with their limits explained (1.1.7), all relevant options discussed even when the local service does not offer them (1.1.9), an assessment by both a specialist surgical oncologist and a specialist clinical oncologist (1.3.5), and an explicit conversation about sexual function, physical appearance, continence and other aspects of masculinity with the man and, if he wishes, his partner (1.1.12).","refs":["active-surveillance","robotic-surgery","hypofractionated-radiotherapy","brachytherapy","protect","psa","gleason-grade-group","cambridge-prognostic-group","percentage-gleason-pattern-4","cribriform-prostate-cancer","mp-mri","multidisciplinary-tumour-board"],"guideline":{"version":"NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"}},{"setting":"If you choose radiotherapy: the schedule, and the hormone therapy that comes with it","approach":"Choosing radiotherapy is choosing a schedule and a course of hormone therapy at the same time, and men are often surprised by the second part. On the schedule, NICE NG131 (1.3.19) says to offer hypofractionated radiotherapy, 60 Gy in 20 fractions, using image-guided intensity modulated radiation therapy unless contraindicated, with conventional radiotherapy, 74 Gy in 37 fractions, reserved for people who cannot have the shorter course. Twenty visits over four weeks is therefore the standard rather than a lesser version of it. NG131 (1.3.24) says to consider adding a brachytherapy boost, where radioactive sources are placed in the prostate itself, for CPG 2 to 5, and (1.3.25) not to offer brachytherapy alone at CPG 4 and 5, so whether a boost is available is a question about the centre. On the hormone therapy, NG131 (1.3.21) says to offer radical radiotherapy combined with androgen deprivation therapy rather than either alone for CPG 2, 3, 4 and 5, (1.3.22) six months of it before, during or after the radiotherapy, and (1.3.23) to consider continuing for up to 3 years at CPG 4 and 5 while discussing the benefits and risks of that with the person. This matters because almost everything men describe afterwards as the effect of radiotherapy is the effect of the hormone therapy: the hot flushes, the loss of sex drive, the weight around the waist, the tiredness. The radiotherapy's own signature is in the bowel and the bladder in the weeks around treatment, and in the small late risks: NG131 (1.3.6) asks that people are told about the small increase in the risk of colorectal cancer after radical external beam radiotherapy, and (1.3.42) that anyone with signs of radiation-induced enteropathy is cared for by a team with expertise in it. For high-risk disease starting long-term hormone therapy, NG131 (1.3.26) asks for a separate discussion about adding six cycles of docetaxel, with box 3 setting out both sides plainly: clear evidence that progression is delayed by about a year, a five-year survival difference of 84 against 80 out of 100 that might be chance, and 15 out of 100 developing a fever from a low white count with 1 in 100 dying of an infection they might not otherwise have had.","refs":["hypofractionated-radiotherapy","brachytherapy","sbrt","docetaxel","stampede","chhip","curative-intent"],"guideline":{"version":"NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"}},{"setting":"Living with hormone therapy: hot flushes, bones, heart, weight and mood, and what is offered for each","approach":"Hormone therapy is the longest part of this illness for most men and the least well covered. It works by taking testosterone away, and testosterone was doing a great many other things. The effects last for as long as the treatment does, and Prostate Cancer UK says that after stopping it can take several months to several years for them to settle, while an orchidectomy cannot be reversed at all. Hot flushes are the commonest complaint: NICE NG131 (1.4.3) says to offer medroxyprogesterone 20 mg a day for an initial 10 weeks and to evaluate the effect at the end, and (1.4.4) to consider cyproterone acetate 50 mg twice a day for 4 weeks if that fails or is not tolerated; in a randomised trial of 309 men the median daily hot-flush score fell by 83.7 percent on medroxyprogesterone and 94.5 percent on cyproterone at one month, against 47.2 percent on venlafaxine. NG131 (1.4.5) also says plainly that there is no good-quality evidence for complementary therapies here. Bone thinning starts in the first year and increases with time on treatment: in 50,613 men, 19.4 percent of those on androgen deprivation surviving at least five years had a fracture against 12.6 percent of those not on it. NICE's four bone sentences run in a specific order: (1.4.12) do not routinely offer bisphosphonates to prevent osteoporosis, (1.4.13) consider assessing fracture risk, (1.4.14) offer bisphosphonates to those who have osteoporosis, and (1.4.15) consider denosumab where bisphosphonates are contraindicated or not tolerated. A DEXA scan is how the question is answered. On the heart and the metabolism, in 73,196 Medicare enrollees GnRH agonist use carried adjusted hazard ratios of 1.44 for new diabetes, 1.16 for coronary heart disease, 1.11 for myocardial infarction and 1.16 for sudden cardiac death; in the HERO trial, major adverse cardiovascular events occurred in 2.9 percent of 622 men on oral relugolix against 6.2 percent of 308 on leuprolide over 48 weeks. Prostate Cancer UK suggests general health checks roughly every six months: weight, blood pressure, cholesterol and a diabetes check. Body composition changes: muscle goes, fat arrives, particularly at the waist, and joint and muscle aches follow. NICE NG131 (1.4.18) says to tell people that fatigue is a recognised effect of the therapy and might not be the cancer, and (1.4.19) to offer supervised resistance and aerobic exercise at least twice a week for 12 weeks to reduce fatigue and improve quality of life, which is the single most concrete offer in this section. On mood, Prostate Cancer UK says hormone therapy itself can cause tearfulness, mood swings, low mood, anxiety and depression, and a meta-analysis of 18 studies in 168,756 men found a 41 percent higher risk of depression on androgen deprivation. Memory and concentration change too, though the evidence for a direct cause is weak. Gynaecomastia has its own answer: NG131 (1.4.16) says to offer prophylactic radiotherapy to both breast buds within the first month for people starting long-term bicalutamide monotherapy, a single 8 Gy fraction, with weekly tamoxifen considered if that does not work. And where treatment is long-term and not adjuvant, NG131 (1.4.1) says to consider intermittent therapy, discussing the limited evidence for a reduction in side effects and the effect on progression, with PSA measured every 3 months and treatment restarted at 10 nanogram/ml or above.","refs":["adt","hot-flushes-on-hormone-therapy","treatment-induced-bone-loss","gynaecomastia","relugolix","abiraterone","enzalutamide","bicalutamide","denosumab","zoledronic-acid","cancer-related-fatigue","exercise-during-chemotherapy","psycho-oncology"],"guideline":{"version":"NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"}},{"setting":"Continence and sexual function: what happens, what help exists, and how to ask for it","approach":"These are the two things men do not raise, so this page raises them first. On continence: most men leak when the catheter comes out after a prostatectomy, usually seven to ten days after the operation, because the operation disturbs the sphincter and the pelvic floor. It improves. In ProtecT, pad use after surgery was 46 percent at six months and 17 percent at six years; radiotherapy barely touched continence at 4 to 5 percent. What helps, in the order the guideline puts it: pelvic floor muscle exercises, started four to six weeks before the operation and restarted as soon as the catheter is out; absorbent pads and pants, sheaths, bed protectors and clamps while things settle; bladder retraining for urgency; and, where it does not settle, medicines, an internal male sling for men leaking two to three pads a day at a year, or an artificial urinary sphincter for men still leaking heavily six months on. NICE NG131 (1.3.39) requires access to specialist continence services, (1.3.40) referral for consideration of an artificial urinary sphincter for intractable stress incontinence, and (1.3.41) rules out bulking agent injections. On sexual function: the figures are in the first row of this page, and they are worth reading with someone rather than alone. What is worth knowing is that the services exist and that starting early works better. NICE NG131 (1.3.36) says to offer access to specialist erectile dysfunction services after radical treatment, (1.3.37) to offer PDE5 inhibitor tablets, and (1.3.38) to offer vacuum devices, intraurethral inserts, penile injections or a penile prosthesis where tablets fail or are contraindicated; (1.4.8) extends the same access to men starting hormone therapy and (1.4.10, 1.4.11) repeats the ladder for them. All of it is free on the NHS whether the erection is wanted for sex or for masturbation, and there is no age limit. Prostate Cancer UK says to try each type of tablet at least eight times before moving on, that injections work within 5 to 10 minutes and often work even when desire is low, that about 3 in 100 implants get infected and roughly 5 in 100 inflatable implants need replacing within ten years, and that an erection lasting more than four hours is priapism and means going straight to accident and emergency. Two other things men are rarely told: the penis can become shorter or curved after surgery, and using a vacuum pump early, alone or with tablets, may help preserve it; and orgasm survives even when ejaculation does not, though it feels different, and some men leak urine at orgasm, which pelvic floor exercises help. Beside all of this NICE NG131 (1.1.13) offers the man and his partner the chance to talk to a healthcare professional experienced in psychosexual issues at any stage, and (1.4.9) considers psychosexual counselling for couples on long-term hormone therapy. Taking that offer is not an admission of anything.","refs":["stress-urinary-incontinence","pelvic-floor-muscle-exercises","artificial-urinary-sphincter","erectile-dysfunction-after-prostate-cancer","priapism","acute-urinary-retention","robotic-surgery","hypofractionated-radiotherapy","psycho-oncology","peer-support-groups","quality-of-life"],"guideline":{"version":"NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"}},{"setting":"A rising PSA after treatment: what it means, how fast it is rising, and what happens next","approach":"After radical treatment the PSA becomes the thing everyone watches, and the waiting for each result has its own name in the clinic. NICE NG131 (1.3.47) says to check it no earlier than 6 weeks after treatment, then at least every 6 months for the first 2 years and at least once a year after that, and (1.3.48) not to do a routine rectal examination while it stays at baseline; (1.3.49) allows remote follow-up after the first 6 months for people with a stable PSA and no significant complications, which for many men means a blood test locally and a phone call. The most useful sentence in the guideline for anyone watching a number go up is (1.3.55): a rising PSA alone should not mean an immediate change in treatment. What matters is the speed, so (1.3.56) asks for the doubling time to be estimated from at least three measurements over at least six months. After a prostatectomy with no known metastases the standard answer is radiotherapy to the prostate bed (1.3.57), often still given with the aim of cure. NG131 (1.3.54) says not to offer routine MRI before salvage radiotherapy but to offer an isotope bone scan if symptoms or PSA trends suggest metastases, and (1.3.58) to consider entry to a clinical trial; in practice a PSMA PET scan is now what localises the disease, and the imaging rows on this page say what it can and cannot see. Hormone therapy is deliberately held back: (1.3.59) says not to offer it routinely for biochemical relapse unless there is symptomatic local progression, proven metastases, or a doubling time of less than three months, which is the guideline protecting men from years of side effects for a number rather than a disease. Where the risk is high, the EMBARK trial is the evidence for adding enzalutamide at this point, and that is a conversation for the multidisciplinary team rather than a default.","refs":["psa-doubling-time","psa","biochemical-recurrence","psma-pet","embark","psa50"],"guideline":{"version":"NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"}},{"setting":"When prostate cancer reaches the bone: cord compression, pain, and protecting the skeleton","approach":"Prostate cancer goes to bone more reliably than almost any other cancer, and the emergency that follows is the one men are least often warned about. Metastatic spinal cord compression happens when deposits in or near the spine press on the spinal cord, and Prostate Cancer UK says about 4 in 100 people with prostate cancer develop it, with the risk highest once the cancer has reached the spine. Untreated it causes nerve damage and can cause paralysis; treated quickly, the risk of that being permanent falls. The signs are worth learning by heart: new, severe or progressive back or neck pain, pain worse on coughing, straining, lying down or at night, tenderness over the spine, a band of pain around the chest or abdomen, pain running down an arm or leg, weakness or unsteadiness in the legs, numbness or pins and needles that does not go away, and any loss of control of the bladder or bowel. NICE NG234 (1.3.2) says to immediately contact the metastatic spinal cord compression coordinator for anyone with a past or current cancer diagnosis and those signs, and to treat it as an oncological emergency; (1.3.3) asks for advice within 24 hours for the pain pattern alone; (1.5.2) asks for an MRI as soon as possible and always within 24 hours; and (1.4.1 to 1.4.3) ask for immobilisation and nursing flat while that is arranged. Prostate Cancer UK adds the practical instruction: do not wait to see if it settles, do not worry that it is the evening or the weekend, ask the team in advance to write down who to contact during the day, at night and at weekends, and if you cannot reach anyone, go to A and E and tell them you have prostate cancer and symptoms of spinal cord compression, because not everyone who sees you will be familiar with it. Alongside the emergency sits the ordinary work of protecting a skeleton. NICE NG131 (1.5.19) says to consider zoledronic acid to prevent or reduce skeletal-related events in hormone-relapsed metastatic disease and (1.5.20) bisphosphonates for pain where painkillers and palliative radiotherapy have not been enough; (1.3.35) says not to offer bisphosphonates to prevent bone metastases developing, and (1.4.12) not to offer them routinely to prevent osteoporosis on hormone therapy. Those are three different questions and NICE gives them three different answers, which is why a single yes or no about bone drugs usually means the wrong question was asked. Radium-223 remains an option for symptomatic bone-only disease that is no longer responding to hormone therapy, with bone protection alongside. A word about words: NICE calls that state hormone-relapsed prostate cancer, many hospitals and papers call it castration-resistant or castrate-resistant, and the three mean the same thing, which is prostate cancer that has started growing again despite testosterone being switched off.","refs":["metastatic-spinal-cord-compression","bone-metastases","radium-223","zoledronic-acid","denosumab","palliative-radiotherapy","pain-management"],"guideline":{"version":"NICE NG234 (2023) and NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng234/chapter/Recommendations"}},{"setting":"A clinical trial or standard treatment","approach":"Prostate cancer has an unusually full trial landscape, because the number of things worth testing keeps growing: radioligands moving earlier in the disease, PARP inhibitor and AR-pathway combinations selected by genetics, T-cell engagers against STEAP1 and KLK2, and, at the other end, trials of how to monitor low-risk disease with fewer biopsies. NICE NG131 names trials at several points rather than as a last resort: (1.3.28) says high-intensity focused ultrasound and cryotherapy should be used for localised disease only in controlled trials comparing them with established treatments, which is the answer to give when a focal treatment is offered privately; (1.3.32 and 1.3.33) say the same about immediate post-operative radiotherapy and adjuvant hormone therapy after prostatectomy; (1.3.58) says to consider trial entry for biochemical relapse; and (1.2.5) restricts mapping transperineal template biopsy at initial assessment to trials. The practical questions are the ordinary ones. The NHS says you can ask your doctor or a patient organisation about trials you may be eligible to join, that you would usually be randomly assigned to the new treatment or to a control group, and that you can leave at any point without giving a reason and without it affecting your care. Worth asking as well: whether taking part means travelling, how many extra scans and biopsies it involves, whether the trial covers travel costs, and what happens to your treatment when the trial ends.","refs":["protect","stampede","embark","multidisciplinary-tumour-board"],"guideline":{"version":"NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"}},{"setting":"When to talk about palliative care","approach":"Palliative care in prostate cancer is often needed for years rather than weeks, because men live a long time with metastatic disease, and the guideline treats it that way. NICE NG131 (1.5.4) says to ensure palliative care is available when needed and is not limited to the end of life, and that care should not be restricted to being associated with hospice care. NG131 (1.5.1) asks for tailored information and access to specialist urology and palliative care teams from the point of a metastatic diagnosis, (1.5.2) for palliative interventions to be integrated at any stage into coordinated care with smooth transitions between settings, (1.5.3) for personal preferences and the preferred place of care to be discussed as early as possible with the man, his partner and his carers, and (1.5.5) for a regular assessment of needs rather than waiting to be asked. In practice this is the team that manages bone pain, fatigue, bowel and bladder symptoms, the fear that arrives with each PSA result, and the conversations nobody else starts. Marie Curie says palliative care can be given alongside treatments aimed at controlling the illness, which is the sentence to quote if a referral feels like a verdict. Alongside it sit the things that keep a life working: Maggie's centres, which are free and need no appointment; Prostate Cancer UK's specialist nurses, one-to-one peer support and online community; a carer's assessment, which is free and is for the person doing the caring rather than the patient; and help with money and work, which is easier to arrange early than late.","refs":["palliative-care","psycho-oncology","peer-support-groups","financial-navigation","survivorship-care-plan","pain-management"],"guideline":{"version":"NICE NG131 (2019, updated December 2021)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"}},{"setting":"Localised prostate cancer, CPG 1 (low risk): the case for doing nothing yet","approach":"Active surveillance, with PSA, multiparametric MRI and repeat biopsy, is the standard and not a compromise. ProtecT randomised 1,643 men with PSA-detected localised disease and found prostate cancer mortality at 15 years of 3.1 percent under monitoring, 2.2 percent after prostatectomy and 2.9 percent after radiotherapy (p=0.53), while 24.4 percent of monitored men were alive at the end of follow-up having never had any treatment. Treatment halves metastasis (9.4 percent monitored against 4.7 and 5.0 percent) but the base rate is low. PIVOT, in a largely PSA-detected United States population, found no significant mortality benefit from surgery over observation at nearly 20 years and more incontinence and erectile dysfunction through 10 years. Padeliporfin vascular-targeted photodynamic therapy is licensed for this population but NICE TA546 does not recommend it.","refs":["protect","pivot","nct01310894","prostate-treatment-choice-localised","prostate-focal-therapy","active-surveillance","decipher-prostate"],"guideline":{"version":"NICE NG131; EAU prostate cancer guidelines","url":"https://www.nice.org.uk/guidance/ng131"}},{"setting":"Localised prostate cancer, CPG 2 to 3 (intermediate risk): surgery or radiotherapy, and how many visits","approach":"Radical prostatectomy and radical radiotherapy give the same cancer outcome and different side-effect shapes; ProtecT's patient-reported outcomes are the best guide to which. If radiotherapy is chosen, moderate hypofractionation is standard: CHHiP found 60 Gy in 20 fractions non-inferior to 74 Gy in 37 (5-year freedom from failure 90.6 against 88.3 percent), PROFIT found 60 Gy in 20 non-inferior to 78 Gy in 39 (85 percent in both arms) and RTOG 0415 found 70 Gy in 28 non-inferior to 73.8 Gy in 41 in low-risk disease. Five-fraction stereotactic body radiotherapy is non-inferior again (PACE-B, 5-year freedom from failure 95.8 against 94.6 percent) at the price of more late grade 2 or higher genitourinary toxicity (26.9 against 18.3 percent). Four to six months of androgen deprivation is added: RTOG 94-08 found 4 months raised 10-year overall survival from 57 to 62 percent, with the benefit confined to intermediate-risk men, and EORTC 22991 found 6 months halved biochemical failure at every radiation dose tested.","refs":["chhip","profit-trial","rtog-0415","pace-b","hypo-rt-pc","rtog-9408","eortc-22991","prostate-radiotherapy-fractionation","prostate-treatment-choice-localised"],"guideline":{"version":"NICE NG131; EAU prostate cancer guidelines","url":"https://www.nice.org.uk/guidance/ng131"}},{"setting":"Localised and locally advanced prostate cancer, CPG 4 to 5 (high risk): radiotherapy with long androgen deprivation","approach":"Radiotherapy plus long-course androgen deprivation, not either alone. SPCG-7 halved 10-year prostate cancer mortality by adding radiotherapy to hormones (11.9 against 23.9 percent) and the NCIC PR.3/MRC PR07 intergroup trial confirmed it in 1,205 men (overall survival hazard ratio 0.70). EORTC 22863 showed the reverse addition works too, raising 10-year overall survival from 39.8 to 58.1 percent. Duration is three years, not six months: EORTC 22961 failed to show non-inferiority for 6 months (5-year mortality 19.0 against 15.2 percent, hazard ratio 1.42), RTOG 92-02 found 28 months better than 4 on every endpoint and better for survival in Gleason 8 to 10 disease (45.1 against 31.9 percent at 10 years), and DART 01/05 GICOR found the same even at radiation doses above 76 Gy. A low-dose-rate brachytherapy boost doubles freedom from biochemical failure at 9 years (83 against 62 percent, ASCENDE-RT) without a survival difference. Adding abiraterone for two years improved 6-year metastasis-free survival from 69 to 82 percent in the STAMPEDE non-metastatic comparison; adding docetaxel improved 4-year overall survival from 89 to 93 percent in RTOG 0521.","refs":["spcg-7","nct00002633","eortc-22863","eortc-22961","rtog-9202","dart-01-05-gicor","ascende-rt","rtog-0521","stampede","prostate-adt-burden","imrt-igrt"],"guideline":{"version":"NICE NG131; EAU prostate cancer guidelines","url":"https://www.nice.org.uk/guidance/ng131"}},{"setting":"After radical prostatectomy with adverse pathology: wait for the PSA rather than irradiate everyone","approach":"An observation policy with early salvage radiotherapy triggered by a rising PSA, not adjuvant radiotherapy. RADICALS-RT (1,396 men), RAVES (333) and GETUG-AFU 17 (424) all found the same, and the prospectively planned ARTISTIC meta-analysis of all 2,153 gave an event-free survival hazard ratio of 0.95 (95 percent confidence interval 0.75 to 1.21), a 1 percentage point difference at 5 years. The gain is in what is avoided: only 33 percent of the RADICALS-RT observation group needed radiotherapy within 8 years, and adjuvant treatment caused more incontinence at 1 year and more grade 3 to 4 urethral stricture (6 against 4 percent). GETUG-AFU 17 measured the same harm larger: late grade 2 or worse genitourinary toxicity 27 against 7 percent and erectile dysfunction 28 against 8 percent. When salvage radiotherapy is given, add androgen deprivation: GETUG-AFU 16 raised 120-month progression-free survival from 49 to 64 percent with 6 months of goserelin, SPPORT raised 5-year freedom from progression from 70.9 to 81.3 percent by adding short-term androgen deprivation and to 87.4 percent by adding pelvic nodal radiotherapy as well, and RADICALS-HD found 24 months better than 6 (10-year metastasis-free survival 78.1 against 71.9 percent) at the cost of more grade 3 toxicity (19 against 14 percent).","refs":["radicals-rt","raves","getug-afu-17","artistic-meta-analysis","getug-afu-16","nct00567580","radicals-hd","rtog-9601","swog-8794","eortc-22911"],"guideline":{"version":"NICE NG131; EAU prostate cancer guidelines","url":"https://www.nice.org.uk/guidance/ng131"}},{"setting":"Metastatic hormone-sensitive prostate cancer: androgen deprivation is never given alone","approach":"Androgen deprivation plus at least one of an androgen receptor pathway inhibitor and docetaxel. Docetaxel: CHAARTED found median overall survival 57.6 against 44.0 months (hazard ratio 0.61) with the benefit concentrated in high-volume disease, and the STAMPEDE docetaxel comparison agreed; GETUG-AFU 15, with 385 men, was the underpowered exception. Androgen receptor pathway inhibitors: abiraterone in LATITUDE and STAMPEDE (hazard ratio for death 0.63 in STAMPEDE's 1,917 men), apalutamide in TITAN (24-month overall survival 82.4 against 73.5 percent, hazard ratio 0.67), enzalutamide in ARCHES and ENZAMET, darolutamide in ARANOTE. Triplets for fit men with de novo high-volume disease: ARASENS added darolutamide to docetaxel and androgen deprivation, PEACE-1 added abiraterone. For low-volume metastatic disease, radiotherapy to the prostate improved survival in the prespecified subgroup of the STAMPEDE radiotherapy comparison. Castration itself can be delivered orally with relugolix (NICE TA995) or, in trials, by transdermal oestradiol patches, which give fewer hot flushes (35 against 86 percent) and better bone density with no excess cardiovascular events. Continuous, not intermittent: SWOG 9346 could not exclude a 20 percent higher risk of death with treatment breaks.","refs":["chaarted","getug-afu-15","latitude","stampede","nct02489318","arches","enzamet","arasens","aranote","peace-1","patch-transdermal-oestradiol","swog-9346","prostate-stampede-arms","prostate-adt-burden"],"guideline":{"version":"NICE TA1110, TA712, TA741, TA1109, TA903; EAU prostate cancer guidelines","url":"https://www.nice.org.uk/guidance/ta1110"}},{"setting":"Hormone-relapsed non-metastatic prostate cancer with a fast-rising PSA","approach":"Apalutamide or darolutamide added to continuing androgen deprivation, for men whose PSA doubling time is 10 months or less. SPARTAN (1,207 men) found median metastasis-free survival 40.5 against 16.2 months with apalutamide (hazard ratio 0.28), and PROSPER and ARAMIS found the same size of effect with enzalutamide and darolutamide. The cost is measurable: in SPARTAN, rash 23.8 against 5.5 percent, hypothyroidism 8.1 against 2.0 percent and fracture 11.7 against 6.5 percent. In England NICE TA740 recommends apalutamide and TA660 darolutamide here; NICE TA580 does not recommend enzalutamide, so one of the three licensed options is not routinely funded. The whole setting is shrinking: men called non-metastatic on CT and bone scan are frequently metastatic on PSMA PET, and the three trials that defined it used conventional imaging.","refs":["nct01946204","prosper","aramis","psma-pet","prostate-uk-drug-approvals"],"guideline":{"version":"NICE TA740, TA660; NICE TA580 does not recommend enzalutamide","url":"https://www.nice.org.uk/guidance/ta740"}},{"setting":"Hormone-relapsed (castration-resistant) metastatic prostate cancer: the order the approved treatments are given in","approach":"An androgen receptor pathway inhibitor if none has been used (COU-AA-302, PREVAIL before chemotherapy; COU-AA-301, AFFIRM after docetaxel); docetaxel with prednisone (TAX 327, median survival 18.9 against 16.5 months against mitoxantrone, with pain relief in 35 against 22 percent); cabazitaxel after docetaxel (TROPIC, 15.1 against 12.7 months; PROSELICA showed 20 mg/m2 is non-inferior to 25 with grade 3 or 4 events in 39.7 against 54.5 percent); olaparib for BRCA-mutated disease after a newer hormonal treatment (NICE TA887; TRITON3 shows the effect is BRCA-dependent and absent in ATM-altered disease); lutetium-177 PSMA radioligand therapy (VISION, TheraP, PSMAfore, but NICE TA930 does not recommend it in England); radium-223 for symptomatic bone-predominant disease without visceral metastases (ALSYMPCA, NICE TA412, only after or instead of docetaxel), now with an overall survival benefit in combination with enzalutamide when bone-protecting agents are given (PEACE-3, 38.2 against 32.6 months). The one hard sequencing rule comes from CARD: after rapid failure of one androgen receptor pathway inhibitor, cabazitaxel beats switching to the other (imaging-based progression-free survival 8.0 against 3.7 months, overall survival 13.6 against 11.0 months).","refs":["cou-aa-301","cou-aa-302","affirm","prevail","tax-327","swog-9916","tropic","proselica","firstana","card","triton3","profound","vision","psmafore","therap","alsympca","peace-3","prostate-crpc-sequencing","prostate-hrr-eligibility"],"guideline":{"version":"NICE TA387, TA377, TA259, TA316, TA101, TA391, TA887, TA412; NICE TA930 does not recommend lutetium-177 vipivotide tetraxetan","url":"https://www.nice.org.uk/guidance/ta930"}},{"setting":"Combinations and strategies that were tested and abandoned","approach":"Checkpoint inhibitors in unselected men do not work: IMbassador250, KEYNOTE-641, KEYNOTE-921, KEYNOTE-991 and CA184-043 between them randomised more than 5,000 men and none improved survival. Anti-angiogenic drugs do not work: CALGB 90401 with bevacizumab and COMET-1 with cabozantinib both improved progression endpoints and neither improved survival, and bevacizumab quadrupled treatment-related deaths (4.0 against 1.2 percent). Endothelin A antagonists do not work: SWOG S0421 and ENTHUSE M1 were both flatly negative. Radium-223 must not be combined with abiraterone without bone protection: ERA 223 found fractures in 29 against 11 percent and no benefit. Two drugs improved radiographic progression-free survival substantially and did nothing for survival, orteronel in ELM-PC 4 and tasquinimod in 10TASQ10, which is why an imaging endpoint alone is not accepted here.","refs":["imbassador250","keynote-921","keynote-641","keynote-991","ca184-043-ipilimumab","calgb-90401","comet-1","swog-s0421-atrasentan","enthuse-m1-zibotentan","ready-dasatinib","era-223","elm-pc-4-orteronel","tasquinimod-10tasq10","prostate-failed-programmes"],"guideline":{"version":"Read from the primary publications; none of these is recommended in any guideline","url":"https://uroweb.org/guidelines/prostate-cancer"}}],"stateOfArt":["Radioligand therapy across the metastatic continuum: 177Lu-PSMA-617 approved post-taxane (2022), pre-taxane (2025), and at first metastatic diagnosis with ARPI (31 July 2026).","Triplet therapy (ADT + ARPI + docetaxel) for high-volume de novo disease, with OS HR ~0.7 (ARASENS, PEACE-1).","Genotype-directed doublets: PARP inhibitor + ARPI for HRR-mutant (OS benefit in TALAPRO-2) and capivasertib + abiraterone for PTEN-deficient disease (2026).","Diagnostic pathway rebuilt around MRI-first biopsy and PSMA PET staging; active surveillance is default for low-risk disease.","AI pathology (ArteraAI Prostate) is FDA-authorised to predict who benefits from adding hormone therapy to radiation.","First immunotherapies with real activity: STEAP1 and KLK2 T-cell engagers in phase 3, after checkpoint inhibitors failed in unselected disease.","The androgen receptor is reactivated by five different routes and most men with castration-resistant disease have more than one: amplification of the gene in about half of castration-resistant cohorts against 1% of untreated primaries, amplification of an enhancer 624 kb upstream in 81% of deeply sequenced metastases, ligand-binding-domain mutation in 13.7 to 18.0%, the AR-V7 splice variant, and raised receptor expression with no genomic change at all.","Stage moves every frequency in this disease more than ancestry or assay does. TP53 runs from 3.4% in localised whole genomes to 41% at rapid autopsy, AR amplification from 1.0% to 57%, PTEN deletion from 12% to 41%. A prostate cancer percentage quoted without its disease state is not usable.","DNA repair is the one axis that changes both treatment and a family's future: inherited mutations in 11.8% of 692 men with metastatic disease, led by BRCA2 at 5.3%, with no difference by family history or age, which is why germline testing is offered to everyone with metastatic disease.","The four PARP inhibitor routes ask for four different gene lists, from BRCA2 alone to a 14-gene panel, and the response evidence does not spread evenly across them: in PROfound, confirmed response was 56% with BRCA2, 10% with ATM and 6% with CDK12.","Mismatch repair deficiency is present in 3.1% of prostate cancers and is the only setting in this disease where checkpoint blockade gives durable responses; one carrier in five also has Lynch syndrome, and in prostate the gene is usually broken by a complex MSH2 or MSH6 rearrangement rather than by MLH1 methylation.","PSMA PET replaced CT and bone scan on accuracy, 92% against 65% in a randomised comparison, and it is the entry ticket for radioligand therapy, but about three men in ten screened for that treatment are ineligible because parts of their tumour no longer express the target.","The way out of androgen receptor dependence is a change of cell identity, not a mutation in the pathway. It requires loss of both RB1 and TP53, it is epigenetic before it is genetic, and it leads either to a neuroendocrine programme or to an androgen receptor-null, neuroendocrine-null state that runs on FGF and MAPK signalling.","Plasma works better here than in most cancers because the metastases are in bone: tumour DNA is detectable in 94% of men with advanced disease, BRCA concordance with tissue is 93%, and plasma sees the polyclonal androgen receptor and reversion events one biopsy cannot."],"history":[{"year":1941,"title":"A cancer is shown to depend on a hormone","note":"Huggins and Hodges castrated men with metastatic prostate cancer, or gave them oestrogen, and the disease regressed; androgen injection made it worse. The first demonstration that a human cancer depends on a circulating hormone, and the origin of systemic cancer therapy. Huggins shared the 1966 Nobel Prize for it.","refs":["paper-huggins-hodges-castration-serum-phosphatases-prostate-1941","androgen-deprivation"]},{"year":1966,"title":"Gleason grading system published","refs":["gleason-grade-group"]},{"year":1986,"title":"PSA test approved for monitoring; screening spreads in the 1990s","refs":["psa"]},{"year":1987,"title":"Prostate-specific antigen becomes a marker","note":"Stamey measured the antigen in 2,200 samples from 699 patients: it tracked tumour volume, fell to undetectable after prostatectomy with a half-life of 2.2 days, and detected recurrence. The same paper warned that it is raised in benign prostatic hyperplasia and is not specific.","refs":["paper-stamey-psa-serum-marker-nejm-1987"]},{"year":1991,"title":"The 4.0 threshold, and the start of population testing","note":"Catalona screened 1,653 healthy men over 50 and biopsied those at or above 4.0 micrograms per litre. Rectal examination alone would have missed 12 of the 37 cancers. Testing spread through primary care over the following decade with no randomised evidence that it saved lives.","refs":["paper-catalona-psa-screening-test-nejm-1991"]},{"year":1995,"title":"Castration resistance is shown to be an adaptation, not an escape","note":"Visakorpi found androgen receptor gene amplification in 7 of 23 tumours recurring on androgen deprivation and in none of the pre-treatment samples from the same men. Chen showed in 2004 that receptor overexpression alone is necessary and sufficient to convert sensitive disease to resistant, and turns antagonists into agonists.","refs":["paper-visakorpi-androgen-receptor-amplification-nat-genet-1995","paper-chen-androgen-receptor-overexpression-antiandrogen-resistance-nat-med-2004"]},{"year":1995,"title":"The receptor can also be rewired to read the wrong hormone","note":"In the same year as the amplification finding, ligand-binding-domain mutations that let progesterone, oestrogen and the antiandrogen itself switch the receptor on are found in 5 of 10 androgen-independent cancers, the second of the five routes out of castration.","refs":["paper-taplin-ar-mutation-androgen-independent-prostate-nejm-1995","androgen-receptor"]},{"year":1997,"title":"The map that made PSMA imaging possible","note":"An immunohistochemical survey shows PSMA is detectable in prostatic epithelium, duodenal mucosa and some renal tubules and almost nowhere else, while falling in dedifferentiated disease, predicting both the treatment and its limits.","refs":["paper-silver-psma-expression-normal-malignant-tissues-ccr-1997","psma"]},{"year":2004,"title":"The first drug to extend survival after hormone therapy fails","note":"TAX 327 gave median survival of 18.9 months with three-weekly docetaxel against 16.5 with mitoxantrone, and improved pain and quality of life; SWOG 9916 reported 17.5 against 15.6 months in the same issue. The end of therapeutic nihilism in castration-resistant disease.","refs":["paper-tannock-tax-327-docetaxel-prednisone-nejm-2004","paper-petrylak-swog-9916-docetaxel-estramustine-nejm-2004","docetaxel"]},{"year":2004,"title":"More receptor is enough on its own","note":"A modest rise in androgen receptor expression, with no mutation, is shown to be necessary and sufficient for antiandrogen resistance and to turn antagonists into agonists, which is the argument that produced abiraterone and enzalutamide.","refs":["paper-chen-androgen-receptor-overexpression-antiandrogen-resistance-nat-med-2004","androgen-receptor"]},{"year":2005,"title":"A gene fusion is found in a common carcinoma","note":"Tomlins found TMPRSS2 fused to ERG or ETV1 in 23 of 29 prostate tumours, putting a growth gene under the control of the hormone the prostate lives in. The first recurrent rearrangement described in a common solid cancer, and still without a drug twenty years later.","refs":["paper-tomlins-tmprss2-ets-fusion-science-2005","erg","tmprss2"]},{"year":2008,"title":"Castration-resistant disease is proved to be still hormone driven","note":"Attard's phase 1 of abiraterone in 21 men resistant to multiple hormonal therapies produced prostate-specific antigen falls of at least 50 percent in 12 of them, lasting up to at least 578 days. The disease was renamed from hormone-refractory to castration-resistant on the strength of results like this.","refs":["paper-attard-abiraterone-phase-1-cyp17-jco-2008"]},{"year":2009,"title":"The two screening trials report on the same day and disagree","note":"ERSPC found a 20 percent reduction in prostate cancer mortality, at 1,410 men screened and 48 extra cancers treated per death prevented. PLCO found no difference, with control-group screening at 52 percent by year six. Welch and Albertsen counted 1,305,600 extra United States diagnoses and 1,004,800 definitive treatments since 1986.","refs":["erspc","plco-prostate","paper-schroder-erspc-screening-mortality-nejm-2009","paper-andriole-plco-prostate-screening-nejm-2009","paper-welch-albertsen-psa-era-diagnosis-treatment-jnci-2009","paper-draisma-lead-time-overdiagnosis-psa-jnci-2009"]},{"year":2010,"title":"A second line opens","note":"TROPIC gave cabazitaxel after docetaxel: 15.1 against 12.7 months, with grade 3 or higher neutropenia in 82 percent. Prostate cancer became a sequencing problem rather than a single-treatment disease.","refs":["paper-de-bono-tropic-cabazitaxel-lancet-2010"]},{"year":2010,"title":"Copy-number burden as a risk measure","note":"Profiling 218 tumours on three platforms identifies NCOA2 as an oncogene in 11% and shows that counting copy-number changes separates high- from low-risk disease beyond Gleason score.","refs":["paper-taylor-integrative-genomic-profiling-cancer-cell-2010","ncoa2"]},{"year":2011,"title":"Abiraterone approved; enzalutamide follows in 2012","note":"Proof that castration-resistant disease is still AR-driven.","refs":["abiraterone","enzalutamide"]},{"year":2011,"title":"Neuroendocrine prostate cancer gets a molecular identity","note":"AURKA and MYCN are co-amplified in 40% of neuroendocrine prostate cancers against 5% of adenocarcinomas, and Aurora kinase inhibition switches off the neuroendocrine programme in models.","refs":["paper-beltran-nepc-aurka-mycn-cancer-discov-2011","aurka","mycn"]},{"year":2012,"title":"Screening is recommended against, and enzalutamide arrives","note":"The United States task force issued a grade D recommendation against prostate-specific antigen screening at any age; it moved men aged 55 to 69 to grade C in 2018. In the same year AFFIRM reported enzalutamide after chemotherapy, 18.4 against 13.6 months, with a prostate-specific antigen response rate of 54 percent against 2 percent.","refs":["paper-moyer-uspstf-prostate-screening-ann-intern-med-2012","paper-uspstf-prostate-screening-jama-2018","paper-scher-affirm-enzalutamide-nejm-2012","paper-beer-prevail-enzalutamide-nejm-2014"]},{"year":2012,"title":"The fusion-negative half of the disease is named","note":"Exome sequencing of 112 tumours makes SPOP the commonest point mutation in prostate cancer and shows SPOP-mutant tumours never carry an ETS fusion; rapid-autopsy sequencing of 50 lethal cancers adds CHD1 deletion, FOXA1 mutation and the chromatin genes that partner the androgen receptor.","refs":["paper-barbieri-spop-foxa1-med12-prostate-nat-genet-2012","paper-grasso-mutational-landscape-lethal-crpc-nature-2012","spop","foxa1"]},{"year":2013,"title":"Radium-223: first alpha emitter approved (ALSYMPCA)","refs":["radium-223","alsympca"]},{"year":2013,"title":"An inherited BRCA mutation is shown to change the disease","note":"Among 2,019 men, carriers present at higher grade and stage and live 8.6 years from diagnosis against 15.7 for non-carriers, which is why a carrier's localised disease is treated rather than watched.","refs":["paper-castro-germline-brca-prostate-outcomes-jco-2013","brca"]},{"year":2014,"title":"The first predictive resistance marker","note":"Antonarakis found AR-V7, an androgen receptor lacking the part the drugs bind, in circulating tumour cells: a zero percent prostate-specific antigen response rate to enzalutamide and abiraterone in the men who carried it, against 53 and 68 percent in those who did not.","refs":["paper-antonarakis-ar-v7-resistance-nejm-2014"]},{"year":2014,"title":"The tumours that change type get a morphological classification","note":"The Prostate Cancer Foundation working committee publishes the six categories that separate incidental neuroendocrine staining from small cell carcinoma, which is what makes treatment-emergent neuroendocrine disease countable at all.","refs":["paper-epstein-neuroendocrine-prostate-morphologic-classification-ajsp-2014"]},{"year":2015,"title":"CHAARTED and STAMPEDE: docetaxel at first metastatic diagnosis","refs":["chaarted","stampede"]},{"year":2015,"title":"The genome is classified, and DNA repair becomes a target","note":"TCGA put 74 percent of 333 primary tumours into seven subtypes and found DNA repair inactivation in 19 percent; the Stand Up To Cancer cohort sequenced 150 metastatic biopsies and found BRCA2, BRCA1 and ATM aberrations in 19.3 percent; TOPARP-A treated 50 unselected men with olaparib and 14 of the 16 with DNA repair defects responded. Gundem showed metastases seed other metastases.","refs":["paper-tcga-molecular-taxonomy-primary-prostate-cell-2015","paper-robinson-integrative-clinical-genomics-advanced-prostate-cell-2015","paper-mateo-toparp-a-olaparib-dna-repair-nejm-2015","paper-gundem-evolutionary-history-lethal-metastatic-prostate-nature-2015"]},{"year":2016,"title":"ProtecT validates active surveillance","refs":["protect","active-surveillance"]},{"year":2016,"title":"Inherited DNA repair faults turn out to be common and unpredictable","note":"Pritchard found presumed deleterious germline DNA repair mutations in 11.8 percent of 692 men with metastatic prostate cancer, BRCA2 in 5.3 percent, with no relation to family history or age at diagnosis. The argument for testing every man with metastatic disease rather than selecting by family history.","refs":["paper-pritchard-inherited-dna-repair-metastatic-prostate-nejm-2016"]},{"year":2016,"title":"The lineage change is mapped, and it is epigenetic before it is genetic","note":"Methylation separates neuroendocrine from castration-resistant adenocarcinoma far more sharply than mutations do, in a pattern fitting divergent clonal evolution from a common ancestor rather than a late mutational event.","refs":["paper-beltran-nepc-divergent-evolution-nat-med-2016"]},{"year":2017,"title":"LATITUDE and STAMPEDE: abiraterone in mHSPC","refs":["latitude","stampede"]},{"year":2017,"title":"Resistance by changing cell type, and imaging moves in front of the biopsy","note":"Mu and Ku showed that losing TP53 and RB1 lets a prostate cancer cell switch on SOX2 and stop needing the androgen receptor, reversibly in the laboratory. PROMIS showed multiparametric magnetic resonance imaging is 93 percent sensitive for clinically significant cancer against 48 percent for standard biopsy, and could spare a quarter of men a biopsy.","refs":["paper-mu-sox2-lineage-plasticity-science-2017","paper-ahmed-promis-multiparametric-mri-lancet-2017","paper-ku-rb1-trp53-lineage-plasticity-science-2017"]},{"year":2017,"title":"Plasma gets a threshold, and PARP resistance gets a mechanism","note":"Above a 2% tumour fraction, plasma reproduces every somatic mutation found in a matched metastatic biopsy, which is the number that makes a liquid biopsy reportable in this disease; in the same year BRCA2 reversion is identified as the mechanism of PARP inhibitor resistance.","refs":["paper-wyatt-ctdna-tissue-concordance-mcrpc-jnci-2017","paper-quigley-brca2-reversion-cfdna-parp-resistance-cancer-discov-2017"]},{"year":2018,"title":"PRECISION: MRI before biopsy","refs":["precision-mri","mp-mri"]},{"year":2018,"title":"Two long-running localised trials read out, and the disparity question is reframed","note":"SPCG-4 at 29 years: surgery cut prostate cancer death by 45 percent in clinically detected disease and added a mean 2.9 years of life. PIVOT at 19.5 years, in a largely screen-detected population, found no significant difference. Dess showed that once treatment and access are equal, the excess prostate cancer mortality in Black men largely disappears while the excess other-cause mortality does not.","refs":["paper-bill-axelson-spcg-4-29-year-nejm-2018","paper-wilt-pivot-prostatectomy-observation-nejm-2017","paper-dess-black-race-prostate-mortality-jama-oncol-2019","paper-teply-restore-bipolar-androgen-therapy-lancet-oncol-2018"]},{"year":2018,"title":"The enhancer nobody was looking at, and the long tail","note":"Deep whole genomes of 101 metastases find the AR upstream enhancer amplified in 81% of men, invisible to exome panels; reanalysis of 1,013 exomes finds 97 driver genes, 70 of them new, most below 3%.","refs":["paper-quigley-structural-variation-mcrpc-cell-2018","paper-armenia-long-tail-oncogenic-drivers-prostate-nat-genet-2018","androgen-receptor"]},{"year":2019,"title":"Rare but real: microsatellite instability, and PSMA PET measured properly","note":"Microsatellite instability-high or mismatch repair deficient disease is found in 3.1% of 1,033 men, with durable checkpoint inhibitor responses in 6 of 11 treated; gallium-68 PSMA-11 PET is shown prospectively to localise recurrence in 75% of 635 men with a rising PSA. RB1 alteration emerges as the only genomic marker independently predicting shorter survival in castration-resistant disease.","refs":["paper-abida-msi-prostate-checkpoint-blockade-jama-oncol-2019","paper-fendler-psma-pet-biochemical-recurrence-jama-oncol-2019","paper-abida-genomic-correlates-outcome-mcrpc-pnas-2019","psma","rb1"]},{"year":2020,"title":"PSMA PET approved; PROfound approves olaparib for HRR-mutant mCRPC","refs":["ga68-psma-11","propsma","profound","olaparib"]},{"year":2020,"title":"PSMA PET replaces conventional staging","note":"In 302 randomised men, PSMA PET-CT is 27% more accurate than CT with bone scan, changes management twice as often and delivers less than half the radiation.","refs":["paper-propsma-hofman-lancet-2020","psma"]},{"year":2021,"title":"VISION: 177Lu-PSMA-617 improves survival; TheraP beats cabazitaxel on response","refs":["vision","therap"]},{"year":2021,"title":"Immunotherapy is measured and found wanting, and sequence is shown to matter","note":"KEYNOTE-199 gave objective response rates of 5 and 3 percent with pembrolizumab and PD-L1 predicted nothing, consistent with a median tumour mutational burden of 2.6 mutations per megabase. TRANSFORMER found identical progression-free survival for high-dose testosterone and enzalutamide and a difference of 8.6 months in progression-free survival through crossover depending on which came first.","refs":["paper-antonarakis-keynote-199-pembrolizumab-jco-2020","paper-chung-comprehensive-genomic-profiling-prostate-jco-po-2019","paper-denmeade-transformer-bipolar-androgen-therapy-jco-2021","paper-conti-trans-ancestry-gwas-prostate-nat-genet-2021"]},{"year":2021,"title":"Plasma at scale, and the noise it carries","note":"Circulating tumour DNA is detectable in 94% of 3,334 men with advanced prostate cancer and agrees with tissue on BRCA mutations 93% of the time; in parallel, clonal haematopoiesis is shown to account for almost half the somatic repair-gene variants found in plasma, most often in ATM.","refs":["paper-tukachinsky-ctdna-3334-advanced-prostate-ccr-2021","paper-jensen-clonal-haematopoiesis-cfdna-interference-prostate-jama-oncol-2021"]},{"year":2022,"title":"Pluvicto approved; ARASENS establishes triplet therapy","refs":["pluvicto","arasens","darolutamide"]},{"year":2022,"title":"Detecting the lineage change without a biopsy, and measuring the disparity in the genome","note":"Cell-free DNA methylation separates neuroendocrine from castration-resistant adenocarcinoma with near-perfect discrimination in two small cohorts; a 2,069-man single-centre series shows tumour genomes differ by self-reported race after adjusting for clinical factors, with more 8q gain in tumours from Black men and an association between community income and 8q gain.","refs":["paper-berchuck-cfdna-methylation-nepc-detection-ccr-2022","paper-stopsack-prostate-genomes-by-race-ccr-2022"]},{"year":2023,"title":"PARP + ARPI combinations approved (TALAPRO-2, PROpel, MAGNITUDE); EMBARK for biochemical recurrence","refs":["talapro-2","propel","magnitude","embark"]},{"year":2023,"title":"PARP inhibition is confirmed, and the biomarker is shown not to be one thing","note":"TRITON3 randomised 405 men and found 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: no effect. 4,855 men were screened to randomise 405.","refs":["paper-fizazi-triton3-rucaparib-nejm-2023","paper-abida-triton2-rucaparib-brca-jco-2020"]},{"year":2024,"title":"SPLASH: second PSMA radioligand improves rPFS but not OS","refs":["splash","lu177-psma-it"]},{"year":2025,"title":"Pluvicto pre-chemotherapy (PSMAfore); ArteraAI Prostate FDA-authorised; PSMAddition positive; ECLIPSE positive; masofaniten discontinued","refs":["psmafore","artera-ai-prostate","psmaddition","eclipse-psma","masofaniten"]},{"year":2026,"title":"Pluvicto approved in metastatic hormone-sensitive disease (31 July); capivasertib + abiraterone approved for PTEN-deficient disease","refs":["psmaddition","pluvicto","capitello-281","capivasertib"]},{"year":2032,"title":"The platform and registry trials are due to complete","note":"ProBio's study completion is listed for December 2026, PSMAddition for 11 February 2027, CAPItello-281 for 31 March 2027, TALAPRO-3 for 28 August 2027, PROTEUS for 13 October 2028, PEACE III for December 2028, PSMA-DC for 3 October 2031, and STAMPEDE2, with 3,360 men planned, for March 2032.","refs":["prostate-roadmap","psmaddition","capitello-281","nct04821622","nct03767244","nct05939414","stampede"]}],"pipeline":["ac225-psma","ifinatamab-deruxtecan","capivasertib","tarlatamab","yl201","cetrelimab","hs-20093","qlc5508","opevesostat","saruparib","aglatimagene-besadenovec","gotistobart","aaa817","pf-07248144","bnt324","bms-986365","jnj-87189401","rinzimetostat","hrs-4357","fpi-2265","xnw5004","azd6621","azd9750","qlh12016","amo959","rv001v","vudalimab","vb15010","nuv-1511","alphabreak","xaluritamig","xalute","pasritamig","mevrometostat","mevpro-1","lu177-psma-it","eclipse-psma","idea-psma-pet-guided-mdt","idea-alpha-first-mhspc","grpr","mp-mri","active-surveillance","decipher-prostate","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-bipolar-androgen-therapy-phase-3-on-pfs2","idea-prostate-metastatic-presentation-as-the-screening-endpoint","idea-prostate-other-cause-mortality-as-a-reported-service-outcome","idea-prostate-per-lesion-mri-audit-before-focal-treatment"],"openProblems":["Screening trade-off: PSA reduces mortality by ~20% but overdiagnoses; MRI-first and risk-adapted intervals are only partly adopted.","Neuroendocrine / lineage-plastic transformation in 10.5 to 17% of late mCRPC (Kench 2022; 17% of metastatic biopsies in Aggarwal) has no targeted therapy; DLL3 and B7-H3 agents are being borrowed from SCLC.","AR-V7 and N-terminal-domain resistance: masofaniten failed; AR degraders remain preclinical/early.","Radioligand sequencing and resistance: about a tenth of men screen out for PSMA-negative disease on VISION's single-tracer criteria and 31% on TheraP's PSMA plus FDG criteria, heterogeneity, and no proven therapy after 177Lu failure outside trials; Ac-225 supply is the constraint.","Overall survival has been hard to show for PSMA radioligands beyond VISION (SPLASH, PSMAfore, TheraP confounded by crossover).","Immunotherapy: checkpoint inhibitors fail in unselected disease; engagers bring cytokine release and need outpatient models.","Equity: Black men have ~70% higher incidence and double the mortality yet are under-enrolled in trials; earlier, risk-adapted screening is the lever.","Bone health, cardiovascular risk, and cognitive effects of long-term ADT in men living a decade or more.","Five classifications describe one disease and no single document reconciles them. A British man holds a histological type from the WHO 2022 classification, a grade on two scales at once, a TNM stage from an edition his guideline does not name, a Cambridge Prognostic Group from NICE and a disease state from the drug labels. Each is used by a different professional and the mapping between the American and British risk systems is approximate.","The staging system is being outrun by the scanners. TNM 8 set the clinical T category from a finger; MRI and PSMA PET see disease it cannot feel, and the TNM committee's own answer in the ninth edition is to record which scan produced the stage rather than to restage the disease. Two men both labelled stage IV, one by bone scan in 2015 and one by PSMA PET in 2026, do not have the same illness, and survival series that span the change cannot be pooled.","Grading still has an unresolved question at its centre. Whether intraductal carcinoma should be counted when the Gleason grade is assigned is decided differently by the two main urological pathology societies, and the WHO fifth edition declined to endorse either, asking only that pathologists say which convention they used. Grade drives the risk band, which drives the treatment.","Ductal histology has no trial of its own. It presents later, metastasises to unusual sites and survives worse than acinar cancer, and every treatment recommendation for it is borrowed from the disease it is not.","Overdiagnosis is real, unavoidable with the current test, and unquantified to within a factor of thirty: estimates across epidemiological, clinical and autopsy studies range from 1.7 to 67 percent, modelling puts it at 23 to 42 percent of screen-detected cancers in United States calibration and 66 percent in the Rotterdam one, and autopsy studies find prostate cancer in 18.5 to 38.5 percent of men who died of something else.","Overtreatment is the harm that overdiagnosis causes, and it is measured in the men who bear it: about 1 in 5 who have radical prostatectomy develop long-term urinary incontinence and 2 in 3 long-term erectile dysfunction, against about 1.3 prostate cancer deaths and about 3 metastatic cases prevented per 1,000 men screened over roughly 13 years.","Metastatic prostate cancer now has six classes of treatment that extend survival and no randomised evidence about the order to give them in; TRANSFORMER measured a difference of 8.6 months in progression-free survival through crossover between two sequences of the same two treatments, which is larger than the gain most of the individual drugs were licensed on.","The homologous recombination repair gene list is used as one biomarker and is not one: BRCA2 loss predicted response to olaparib in every case in TOPARP-A, ATM alteration gave a hazard ratio of 0.95 in TRITON3, and CDK12-altered tumours, 6 percent of the disease, are infrequently high for genome-wide loss of heterozygosity and are not homologous recombination deficient in the sense PARP inhibitors need.","In a minority of men, treatment turns prostate cancer into a different disease: combined TP53 and RB1 loss allows a switch to an androgen receptor-independent, often neuroendocrine phenotype, found in 17 percent of metastatic biopsies in one prospective cohort, for which there is no approved treatment and no prospective surveillance strategy.","Checkpoint immunotherapy does not work here and nobody can say which few patients it does work in: objective response rates of 5 percent in PD-L1-positive and 3 percent in PD-L1-negative disease, a median tumour mutational burden of 2.6 mutations per megabase, and mismatch repair deficiency in 4 percent of tumours, with durable responses in a subgroup that cannot be identified in advance.","Magnetic resonance imaging is reported as a patient-level test and used as a lesion-level map: sensitivity is 93 percent for whether a man has clinically significant cancer and 65 percent for whether a given significant lesion is seen, with at least one significant focus missed in 34 percent of men and 45 percent of those with multifocal disease, and no service publishes its own per-lesion figure.","The mortality gap that survives equal access is not a cancer gap: after adjustment for treatment and access, Black men in three United States cohorts had no excess prostate cancer mortality at the same stage, and a persistently higher hazard of dying of other causes, in a population treated for years with a hormone therapy that worsens metabolic and bone health.","The TMPRSS2-ERG fusion defines roughly half of all prostate cancers, has been known since 2005, and has produced no treatment; the same is true of the seven-subtype TCGA taxonomy, which leaves a quarter of primary tumours unclassified.","The commonest driver event in advanced prostate cancer, amplification of the AR enhancer 624 kb upstream of the gene, is invisible to every panel used to test for it.","Two of the four PARP inhibitor eligibility lists name genes for which almost no prostate response data exist. Across 142 men in the non-BRCA, non-ATM PROfound cohort, 89 had CDK12 and the remaining eleven genes supplied between one and twelve men each, with no responses; talazoparib's list names a mismatch repair gene, MLH1, and its own label states that no approved test for it exists.","The commonest genomic alteration in the disease, the TMPRSS2-ERG fusion, has no treatment and no prognostic value, and the drivers that might be treatable follow a long tail: 97 significantly mutated genes, 70 of them new, most below 3% prevalence.","AR-V7 is the closest this disease has to a test that chooses between two treatment classes and it is in no label, needs intact circulating tumour cells, and the two available assays disagree on 18% of samples.","Neuroendocrine transformation is recognised late because it is found by biopsying a lesion someone thought to biopsy. The genotype that permits it, combined RB1 and TP53 loss, is knowable in advance, and the non-invasive methylation test that detects it exists only as a research assay in cohorts of a few dozen men.","Clonal haematopoiesis accounts for almost half the somatic DNA repair variants found in plasma from men with advanced prostate cancer, most often in ATM, and the fix, a paired whole-blood control, is not universal.","Prostate cancer genomics is overwhelmingly a description of men of European ancestry. In the one large Chinese cohort the founder event that defines almost half of Western tumours is uncommon, and in a 2,069-man single-centre series tumours from Black men carried more 8q gain, an adverse feature, with community-level income associated with that gain after adjusting for race and ancestry.","PSMA PET has moved staging without anyone yet showing that treating the disease it finds changes survival, which is stage migration operating on a national scale."],"basics":{"symptoms":["Prostate cancer often has no symptoms at first, because it usually starts on the outer part of the gland and does not press on the urethra until it has grown or spread (NHS)","Changes in the way you pee: difficulty starting or straining, a weak flow, stop-start peeing, needing to pee urgently or often, feeling you still need to pee when you have just finished, and getting up in the night (NHS)","Other symptoms: erectile dysfunction, blood in the urine or the semen, and, in advanced disease, lower back pain and losing weight without trying (NHS)","These symptoms far more often mean benign prostatic enlargement, which is very common with age, than cancer; the NHS advice is not that they are alarming but that a change in them should be checked (NHS)","See a GP if you are having trouble peeing or have other symptoms, if you are over 40 and genetic testing has shown you carry a faulty BRCA2 gene, or if you are worried about your risk; you can ask about a PSA test even without symptoms, and the GP will weigh your risk in deciding whether it is the right test for you (NHS)","At the appointment the GP will ask whether anyone in the family has had prostate, pancreatic, ovarian or breast cancer, may examine the prostate with a gloved finger through the back passage, and may offer a PSA blood test with results in one to two weeks (NHS)"],"diagnosis":["Multiparametric MRI is offered first, before any biopsy, for suspected clinically localised prostate cancer, and is reported on a five-point Likert scale rather than PI-RADS (NICE NG131 1.2.2)","MRI-influenced biopsy is offered at Likert 3 or above; at Likert 1 or 2 omitting biopsy can be considered after a shared discussion of the risks and benefits, and systematic biopsy is offered to anyone who still wants one (NG131 1.2.3, 1.2.4)","Mapping transperineal template biopsy is not offered as part of an initial assessment outside a trial (NG131 1.2.5)","After a negative biopsy with an MRI Likert score of 3 or more, the case is discussed at the MDT with a view to repeating the biopsy; after a negative biopsy with Likert 1 or 2, PSA is repeated at 3 to 6 months (NG131 1.2.10, 1.2.12)","CT is considered where MRI is contraindicated and knowing the T or N stage would change management (NG131 1.2.14)","The pathology report gives the histological type, the Gleason score and the grade group, the tumour length in each core, the percentage of Gleason pattern 4 and whether intraductal or invasive cribriform carcinoma is present; on a prostatectomy specimen it adds extraprostatic extension, seminal vesicle invasion, margins and nodes (RCPath G084, October 2024)","Isotope bone scans are not routinely offered in Cambridge Prognostic Group 1 or 2 (NG131 1.2.16)"],"staging":["Five classifications are in use at once and they answer different questions: histology (what it is), grade (how abnormal it looks), TNM stage (how far it has spread), risk band (what those three add up to) and disease state (what it is doing now). A man can be described by all five simultaneously","Grade: Gleason score and grade group together. Group 1 is Gleason 6 or less, group 2 is 3+4=7, group 3 is 4+3=7, group 4 is Gleason 8 (4+4, 3+5 or 5+3), group 5 is Gleason 9 to 10 (RCPath G084, from the ISUP 2014 consensus)","Risk band in the UK: the Cambridge Prognostic Groups 1 to 5, which the MDT assigns to every newly diagnosed localised or locally advanced case, combining grade group, PSA and T stage. NICE writes its whole treatment section in these numbers (NG131 1.2.15, table 1)","Stage: T1 not palpable or visible (T1c is a cancer found on biopsy after a raised PSA), T2 confined within the prostate, T3a through the capsule, T3b into a seminal vesicle, T4 fixed to or invading rectum, sphincter, levator muscles or pelvic wall; N1 any regional pelvic node; M1a non-regional node, M1b bone, M1c elsewhere. There is no pT1 category and the eighth edition removed the substaging of pT2","UK pathology reports stage against UICC TNM 8, which the Royal College of Pathologists dataset names and reprints (G084, October 2024)","TNM 9 was published on 3 July 2025 and UICC recommends it from 1 January 2026. The prostate T, N and M categories are unchanged; the clinical stage grouping was clarified, and reports are now asked to record the imaging method as a suffix, cT2b(mr) for MRI and N1(PET) for a node found on PSMA PET, because prostate is the malignancy most affected by stage migration (Brierley 2026)","NICE NG131 names no TNM edition. Its risk table uses bare T1 to T4, which are identical in the eighth and ninth editions","Disease state, which is not a stage: hormone-sensitive or castration-resistant (which NICE calls hormone-relapsed), metastatic or not, and whether the PSA alone has risen after treatment (biochemical recurrence). Each of these has its own page here","In England 53 percent of prostate cancers with a known stage were diagnosed at stage I or II in 2022, against 37 percent in Scotland in 2023, 57 percent in Northern Ireland and 59 percent in Wales (Cancer Research UK)"],"sources":[{"label":"NICE NG131: prostate cancer, diagnosis and management (recommendations, including the Cambridge Prognostic Group table at 1.2.15)","url":"https://www.nice.org.uk/guidance/ng131/chapter/Recommendations"},{"label":"Royal College of Pathologists G084: dataset for histopathology reports for prostatic carcinoma, version 4, October 2024","url":"https://www.rcpath.org/static/8cc88604-2c8d-4df4-a99542df41c102af/G084-dataset-for-histopathology-reports-for-prostatic-carcinoma.pdf"},{"label":"Brierley et al., International Journal of Cancer 2026: the 9th edition of the UICC TNM classification of malignant tumours, updates and rationale for change (prostate at section 10.1)","url":"https://doi.org/10.1002/ijc.70561"},{"label":"NHS: symptoms of prostate cancer, and what happens at the GP appointment","url":"https://www.nhs.uk/conditions/prostate-cancer/symptoms/"},{"label":"Cancer Research UK: prostate cancer statistics (UK incidence, mortality, survival, stage at diagnosis and route to diagnosis)","url":"https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/prostate-cancer"}]},"prognosis":{"text":"In the United States, 98.2% of men diagnosed with prostate cancer in 2016-2022 were alive five years later, relative to men of the same age without the disease. For the 69% found while confined to the prostate and the 14% with regional spread, five-year relative survival is 100%; for the 9% found with distant spread it is 40.1%. Most prostate cancers grow slowly, and for many men the question is whether treatment is needed at all rather than whether it will work.","sources":[{"label":"SEER Cancer Stat Facts: Prostate Cancer","url":"https://seer.cancer.gov/statfacts/html/prost.html"}]}},"route":"/cancers/prostate/","neighbours":{"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":"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","route":"/roadmaps/prostate-roadmap/"},{"id":"radiopharma-roadmap","kind":"roadmap","name":"Radiopharmaceutical roadmap: iodine → lutetium → actinium","route":"/roadmaps/radiopharma-roadmap/"}],"pairing":[{"id":"ai-pathology-to-adt","kind":"pairing","name":"AI pathology → androgen deprivation duration","route":"/pairings/ai-pathology-to-adt/"},{"id":"beta-then-alpha","kind":"pairing","name":"Beta radioligand → alpha radioligand","route":"/pairings/beta-then-alpha/"},{"id":"proton-vs-imrt","kind":"pairing","name":"Caution: proton therapy vs IMRT","route":"/pairings/proton-vs-imrt/"},{"id":"parp-plus-arpi","kind":"pairing","name":"PARP inhibitor + AR pathway inhibitor (prostate)","route":"/pairings/parp-plus-arpi/"},{"id":"psma-pet-to-rlt","kind":"pairing","name":"PSMA PET → PSMA radioligand therapy","route":"/pairings/psma-pet-to-rlt/"}],"collection":[{"id":"nhs-jewish-brca-testing","kind":"collection","name":"NHS Jewish BRCA Testing Programme","route":"/collections/nhs-jewish-brca-testing/"},{"id":"prostate-cancer-promise","kind":"collection","name":"PROMISE registry: free germline testing in prostate cancer","route":"/collections/prostate-cancer-promise/"},{"id":"prostate-cancer-foundation","kind":"collection","name":"Prostate Cancer Foundation (PCF)","route":"/collections/prostate-cancer-foundation/"},{"id":"src-urotoday","kind":"collection","name":"UroToday","route":"/collections/src-urotoday/"}],"cancer":[{"id":"prostate-bcr","kind":"cancer","name":"Biochemical recurrence of prostate cancer","route":"/cancers/prostate-bcr/"},{"id":"prostate-ductal-adenocarcinoma","kind":"cancer","name":"Ductal adenocarcinoma of the prostate","route":"/cancers/prostate-ductal-adenocarcinoma/"},{"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 cancer","route":"/cancers/prostate-nepc/"},{"id":"prostate-nmcrpc","kind":"cancer","name":"Non-metastatic castration-resistant prostate cancer","route":"/cancers/prostate-nmcrpc/"}],"idea":[{"id":"idea-bio1-adaptive-therapy-platform","kind":"idea","name":"A multi-cancer platform trial of adaptive (dose-holiday) therapy","route":"/ideas/idea-bio1-adaptive-therapy-platform/"},{"id":"idea-fund-intraoperative-imaging-trials","kind":"idea","name":"A pragmatic trial network for intraoperative margin tools, paid on margin reduction","route":"/ideas/idea-fund-intraoperative-imaging-trials/"},{"id":"idea-moon-generics-for-cancer-fund","kind":"idea","name":"A public fund and label pathway to trial generic drugs against cancer","route":"/ideas/idea-moon-generics-for-cancer-fund/"},{"id":"idea-bio2-antimetastatic-endpoint","kind":"idea","name":"A regulatory endpoint for drugs that block spread, not tumours","route":"/ideas/idea-bio2-antimetastatic-endpoint/"},{"id":"idea-tr1-window-of-opportunity-default","kind":"idea","name":"A short pre-surgery drug window as the default early test of new agents","route":"/ideas/idea-tr1-window-of-opportunity-default/"},{"id":"idea-tr1-standing-platform-per-cancer","kind":"idea","name":"A standing platform trial for every major cancer, funded as infrastructure","route":"/ideas/idea-tr1-standing-platform-per-cancer/"},{"id":"idea-bio2-oligometastatic-signature","kind":"idea","name":"A test to tell true oligometastatic disease from hidden widespread spread","route":"/ideas/idea-bio2-oligometastatic-signature/"},{"id":"idea-fund-surgical-video-registry","kind":"idea","name":"A video-based surgical quality registry linking assessed skill to cancer outcomes","route":"/ideas/idea-fund-surgical-video-registry/"},{"id":"idea-alpha-first-mhspc","kind":"idea","name":"Alpha-emitting PSMA therapy at first metastatic diagnosis","route":"/ideas/idea-alpha-first-mhspc/"},{"id":"idea-prev-indolent-lesion-nomenclature-body","kind":"idea","name":"An international body to rename indolent lesions so 'cancer' means something","route":"/ideas/idea-prev-indolent-lesion-nomenclature-body/"},{"id":"idea-bio2-organotropism-atlas","kind":"idea","name":"An organotropism atlas that predicts where a cancer will spread","route":"/ideas/idea-bio2-organotropism-atlas/"},{"id":"idea-prev-reflex-germline-testing","kind":"idea","name":"Automatic germline testing for every cancer type where it changes care","route":"/ideas/idea-prev-reflex-germline-testing/"},{"id":"idea-moon-closed-loop-adaptive-therapy","kind":"idea","name":"Autonomous closed-loop adaptive therapy driven by blood tests and evolutionary models","route":"/ideas/idea-moon-closed-loop-adaptive-therapy/"},{"id":"idea-acc-cardiometabolic-clinic-hormone-therapy","kind":"idea","name":"Cardiometabolic screening and treatment for survivors on long-term hormone therapy","route":"/ideas/idea-acc-cardiometabolic-clinic-hormone-therapy/"},{"id":"idea-moon-certified-decision-aids","kind":"idea","name":"Certified decision aids required for every preference-sensitive cancer decision","route":"/ideas/idea-moon-certified-decision-aids/"},{"id":"idea-bio2-ctc-clearance-go-nogo","kind":"idea","name":"Circulating tumour cell clearance as the phase 2 gate for anti-metastatic drugs","route":"/ideas/idea-bio2-ctc-clearance-go-nogo/"},{"id":"idea-fund-adaptive-radiotherapy-evidence","kind":"idea","name":"Coverage-with-evidence registries for MR-guided and adaptive radiotherapy","route":"/ideas/idea-fund-adaptive-radiotherapy-evidence/"},{"id":"idea-nerve-tumour-blockade","kind":"idea","name":"Cut the nerve supply to tumours with old drugs","route":"/ideas/idea-nerve-tumour-blockade/"},{"id":"idea-acc-embedded-decision-aids","kind":"idea","name":"Decision aids built into the record for every preference-sensitive cancer choice","route":"/ideas/idea-acc-embedded-decision-aids/"},{"id":"idea-bio1-arv7-degrader","kind":"idea","name":"Destroy the truncated androgen receptor that hormone drugs cannot touch","route":"/ideas/idea-bio1-arv7-degrader/"},{"id":"idea-bio1-cfrna-plasticity-tracking","kind":"idea","name":"Detect tumours changing cell type from RNA in the blood","route":"/ideas/idea-bio1-cfrna-plasticity-tracking/"},{"id":"idea-fund-ablation-versus-surgery-trials","kind":"idea","name":"Device-agnostic public trials of ablation technologies against surgery","route":"/ideas/idea-fund-ablation-versus-surgery-trials/"},{"id":"idea-moon-dormancy-eradication-programme","kind":"idea","name":"Eradicate dormant cancer cells: a programme to wake and kill or lock asleep disseminated cells","route":"/ideas/idea-moon-dormancy-eradication-programme/"},{"id":"idea-tr1-adaptive-therapy-randomised-phase-2","kind":"idea","name":"Evolution-guided 'adaptive therapy' dosing tested in randomised phase 2 trials","route":"/ideas/idea-tr1-adaptive-therapy-randomised-phase-2/"},{"id":"idea-tr1-duffy-null-neutrophil-threshold","kind":"idea","name":"Fix the neutrophil count rule that excludes many people of African ancestry","route":"/ideas/idea-tr1-duffy-null-neutrophil-threshold/"},{"id":"idea-bio2-ctc-culture-functional-testing","kind":"idea","name":"Grow blood-borne tumour cells to test drugs on the cells that actually spread","route":"/ideas/idea-bio2-ctc-culture-functional-testing/"},{"id":"idea-bio1-ctc-derived-explants","kind":"idea","name":"Grow models from tumour cells in the blood when a biopsy is impossible","route":"/ideas/idea-bio1-ctc-derived-explants/"},{"id":"idea-prostate-metastatic-presentation-as-the-screening-endpoint","kind":"idea","name":"Judge a prostate screening programme on metastatic presentation, not on incidence or mortality","route":"/ideas/idea-prostate-metastatic-presentation-as-the-screening-endpoint/"},{"id":"idea-bio2-pro-dormancy-therapy","kind":"idea","name":"Keep dormant cells asleep instead of trying to kill them","route":"/ideas/idea-bio2-pro-dormancy-therapy/"},{"id":"idea-dormancy-maintenance-therapy","kind":"idea","name":"Keep them asleep: dormancy maintenance as adjuvant therapy","route":"/ideas/idea-dormancy-maintenance-therapy/"},{"id":"idea-moon-cold-to-hot-programme","kind":"idea","name":"Make every cold tumour hot: a coordinated programme to reprogramme immune-excluded tumours","route":"/ideas/idea-moon-cold-to-hot-programme/"},{"id":"idea-acc-hypofractionation-default-lmic","kind":"idea","name":"Make one-week radiotherapy the default in overloaded systems","route":"/ideas/idea-acc-hypofractionation-default-lmic/"},{"id":"idea-fund-device-technique-registry","kind":"idea","name":"Mandatory staged registries for new surgical techniques before wide adoption","route":"/ideas/idea-fund-device-technique-registry/"},{"id":"idea-prev-modern-autopsy-reservoir-studies","kind":"idea","name":"Modern autopsy studies to measure how much silent cancer people carry","route":"/ideas/idea-prev-modern-autopsy-reservoir-studies/"},{"id":"idea-moon-indolence-classifiers-with-screening","kind":"idea","name":"Molecular indolence classifiers bundled with every screening programme","route":"/ideas/idea-moon-indolence-classifiers-with-screening/"},{"id":"idea-prev-mri-first-prostate-screening-prs","kind":"idea","name":"MRI-first prostate screening with genetic pre-selection","route":"/ideas/idea-prev-mri-first-prostate-screening-prs/"},{"id":"idea-fund-open-source-repurposing-leads","kind":"idea","name":"Patent-free open-source development of repurposed and off-patent cancer drugs","route":"/ideas/idea-fund-open-source-repurposing-leads/"},{"id":"idea-cost-hypofractionation-payment","kind":"idea","name":"Pay for a course of radiotherapy, not for each fraction","route":"/ideas/idea-cost-hypofractionation-payment/"},{"id":"idea-bio2-exercise-reimbursement","kind":"idea","name":"Pay for supervised exercise the way we pay for drugs","route":"/ideas/idea-bio2-exercise-reimbursement/"},{"id":"idea-fund-course-based-radiotherapy-payment","kind":"idea","name":"Pay per course of radiotherapy, not per session, so short courses are not penalised","route":"/ideas/idea-fund-course-based-radiotherapy-payment/"},{"id":"idea-fund-omission-deescalation-trials","kind":"idea","name":"Payer-funded trials that omit surgery or radiotherapy in low-risk patients","route":"/ideas/idea-fund-omission-deescalation-trials/"},{"id":"idea-fund-proton-coverage-with-evidence","kind":"idea","name":"Pooled coverage-with-evidence for proton therapy across all centres","route":"/ideas/idea-fund-proton-coverage-with-evidence/"},{"id":"idea-tr1-pre-consented-cohort-randomisation","kind":"idea","name":"Pre-consented cohorts that can be randomised to future trials (TwiCs)","route":"/ideas/idea-tr1-pre-consented-cohort-randomisation/"},{"id":"idea-cost-low-dose-abiraterone-food","kind":"idea","name":"Prescribe a quarter dose of abiraterone with breakfast","route":"/ideas/idea-cost-low-dose-abiraterone-food/"},{"id":"idea-prev-prostate-as-triggered-biopsy","kind":"idea","name":"Prostate active surveillance without scheduled biopsies: MRI and blood tests 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-tr2-psma-volume-qualification","kind":"idea","name":"Qualify PSMA PET tumour volume as a validated imaging biomarker","route":"/ideas/idea-tr2-psma-volume-qualification/"},{"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-moon-image-guided-surgery-everywhere","kind":"idea","name":"Real-time margin assessment and image-guided surgery as the global standard","route":"/ideas/idea-moon-image-guided-surgery-everywhere/"},{"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-acc-risk-stratified-follow-up","kind":"idea","name":"Risk-stratified follow-up: low-risk survivors to primary care with fast re-entry","route":"/ideas/idea-acc-risk-stratified-follow-up/"},{"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-moon-sexual-health-as-toxicity-domain","kind":"idea","name":"Sexual health assessed and treated as a standard toxicity domain","route":"/ideas/idea-moon-sexual-health-as-toxicity-domain/"},{"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-exercise-as-adjuvant","kind":"idea","name":"Structured exercise prescribed like a drug in all curative-intent cancer care","route":"/ideas/idea-exercise-as-adjuvant/"},{"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-total-body-pet-dosimetry","kind":"idea","name":"Total-body PET for personalised radioligand dosing","route":"/ideas/idea-total-body-pet-dosimetry/"},{"id":"idea-bio2-hypoxia-guided-adenosine","kind":"idea","name":"Use a hypoxia scan to pick patients for adenosine-pathway drugs","route":"/ideas/idea-bio2-hypoxia-guided-adenosine/"},{"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-tr1-food-effect-dose-reduction","kind":"idea","name":"Use food effects to cut the dose and cost of oral drugs that absorb better with meals","route":"/ideas/idea-tr1-food-effect-dose-reduction/"},{"id":"idea-bio2-let-rbe-ab-selects-protons","kind":"idea","name":"Use LET, RBE and alpha/beta to decide when protons beat IMRT","route":"/ideas/idea-bio2-let-rbe-ab-selects-protons/"},{"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/"},{"id":"idea-dtc-colonisation-determinants","kind":"idea","name":"What decides which disseminated cells ever colonise?","route":"/ideas/idea-dtc-colonisation-determinants/"},{"id":"idea-bio2-localise-the-mrd","kind":"idea","name":"When the blood test is positive, hunt for the lesion with sensitive imaging","route":"/ideas/idea-bio2-localise-the-mrd/"},{"id":"idea-chip-risk-modifiers","kind":"idea","name":"Which patients' blood clones will become leukaemia after treatment?","route":"/ideas/idea-chip-risk-modifiers/"}],"biomarker":[{"id":"ar-amplification","kind":"biomarker","name":"AR amplification (gene and upstream enhancer)","route":"/biomarkers/ar-amplification/"},{"id":"ar-ligand-binding-domain-mutation","kind":"biomarker","name":"AR ligand-binding-domain mutation (L702H, W742C, H875Y, T878A, F877L)","route":"/biomarkers/ar-ligand-binding-domain-mutation/"},{"id":"ar-v7-splice-variant","kind":"biomarker","name":"AR-V7 splice variant","route":"/biomarkers/ar-v7-splice-variant/"},{"id":"ctdna-tumour-fraction","kind":"biomarker","name":"Circulating tumour DNA fraction (and what a negative plasma result means)","route":"/biomarkers/ctdna-tumour-fraction/"},{"id":"dmmr-ihc","kind":"biomarker","name":"dMMR (mismatch repair deficiency by IHC)","route":"/biomarkers/dmmr-ihc/"},{"id":"brca-germline","kind":"biomarker","name":"Germline BRCA1/2 pathogenic variant (gBRCAm)","route":"/biomarkers/brca-germline/"},{"id":"hrr-gene-mutation","kind":"biomarker","name":"Homologous recombination repair gene mutation in prostate cancer","route":"/biomarkers/hrr-gene-mutation/"},{"id":"hrd-positive","kind":"biomarker","name":"HRD-positive (genomic instability score)","route":"/biomarkers/hrd-positive/"},{"id":"msi-high","kind":"biomarker","name":"MSI-high (microsatellite instability by PCR or sequencing)","route":"/biomarkers/msi-high/"},{"id":"psma-pet-expression","kind":"biomarker","name":"PSMA expression by PET (PSMA-positive)","route":"/biomarkers/psma-pet-expression/"},{"id":"pten-alteration","kind":"biomarker","name":"PTEN alteration (sequencing) and PTEN loss (IHC)","route":"/biomarkers/pten-alteration/"},{"id":"spop-mutation","kind":"biomarker","name":"SPOP mutation","route":"/biomarkers/spop-mutation/"},{"id":"tmb-high","kind":"biomarker","name":"TMB-high (tumour mutational burden >= 10 mutations per 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