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Everything in development, the medicines held by this cancer's subtypes, the open problems and what is being done about them, the roadmaps, and what changed on this record.
What is in development for Prostate cancer, drawn from the whole corpus: 436 items. Drugs are grouped by the most advanced trial phase they have reached anywhere; approved treatments sit under standard of care. Technologies are the methods being tested for this cancer, trials are the studies recorded here, and ideas are proposals not yet in a trial.
4 medicines on record are linked to one of the types below rather than to Prostate cancer itself. Grouped by the type that holds them; each list opens that type's own page.
Screening trade-off: PSA reduces mortality by ~20% but overdiagnoses; MRI-first and risk-adapted intervals are only partly adopted.
Background: Screening. Also on OnCo: Symptoms and red flags · Early detection roadmap.
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.
Background: Circulating tumour DNA (ctDNA), Oligometastatic disease, Organ tropism: seed and soil. Also on OnCo: Atlas of advanced disease · How cancer spreads: the metastasis stages.
AR-V7 and N-terminal-domain resistance: masofaniten failed; AR degraders remain preclinical/early.
Background: Castration-resistant prostate cancer (CRPC), Circulating tumour DNA (ctDNA), Cross-resistance, Drug resistance (primary and acquired), Histologic transformation. Also on OnCo: Resistance: how tumours escape each drug class · Lines of therapy.
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.
Background: Castration-resistant prostate cancer (CRPC), Circulating tumour DNA (ctDNA), Cross-resistance, Drug resistance (primary and acquired), Histologic transformation. Also on OnCo: Resistance: how tumours escape each drug class · Lines of therapy.
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.
Background: Quality of life. Also on OnCo: Side effects by symptom · Checkpoint side effects by organ · Side effect rates across a drug class · Survivorship planner.
Equity: Black men have ~70% higher incidence and double the mortality yet are under-enrolled in trials; earlier, risk-adapted screening is the lever.
Background: Screening. Also on OnCo: Symptoms and red flags · Early detection roadmap.
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.
Background: Circulating tumour DNA (ctDNA), Oligometastatic disease, Organ tropism: seed and soil. Also on OnCo: Atlas of advanced disease · How cancer spreads: the metastasis stages.
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.
Background: Circulating tumour DNA (ctDNA), Oligometastatic disease, Organ tropism: seed and soil. Also on OnCo: Atlas of advanced disease · How cancer spreads: the metastasis stages.
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.
Background: Circulating tumour DNA (ctDNA), Oligometastatic disease, Organ tropism: seed and soil. Also on OnCo: Atlas of advanced disease · How cancer spreads: the metastasis stages.
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.
Background: Circulating tumour DNA (ctDNA), Oligometastatic disease, Organ tropism: seed and soil. Also on OnCo: Atlas of advanced disease · How cancer spreads: the metastasis stages.
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.
Background: Circulating tumour DNA (ctDNA), Oligometastatic disease, Organ tropism: seed and soil. Also on OnCo: Atlas of advanced disease · How cancer spreads: the metastasis stages.
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.
Background: Tumour-agnostic (tissue-agnostic) approval. Also on OnCo: Find a trial · Expert centres.
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.
Also on OnCo: Financial help · Coverage by country · Funding verdicts by country.
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.
Background: Quality of life. Also on OnCo: Side effects by symptom · Checkpoint side effects by organ · Side effect rates across a drug class · Survivorship planner.
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.
Dated changes read from the records linked to this cancer: approvals, regulatory steps, reported trials, guideline versions and milestones. Newest first; no date is inferred.
On EdgeAll 198 changes by month →When this page itself was last checked or edited.
PSMA+ metastatic hormone-sensitive prostate cancer with ARPI (PSMAddition)
Capivasertib approved for use with abiraterone and prednisone in PTEN-deficient metastatic prostate cancer (CAPItello-281); abiraterone itself was already approved
PTEN-deficient metastatic prostate cancer with abiraterone (CAPItello-281)
FDA approves capivasertib with abiraterone and prednisone for PTEN-deficient androgen pathway modulation-naïve or -sensitive prostate cancer
Pylarify TruVu formulation