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Prostate cancer that keeps growing even though testosterone has been reduced to castrate levels.
Defined by PSA or radiographic progression with testosterone <50 ng/dL. Mechanisms: AR amplification and mutations, AR-V7 splice variants, intratumoural androgen synthesis, glucocorticoid receptor bypass, lineage plasticity to neuroendocrine phenotype. Since 2026 the FDA label language 'androgen pathway modulation-naive or -sensitive' replaces 'hormone-sensitive'.
About three quarters of cancers arise in the peripheral zone at the back of the gland, the part a finger or a biopsy needle reaches; drainage is to the obturator and iliac nodes.
Same organ: Ductal adenocarcinoma of the prostate, Localised prostate cancer, very low and low risk, Localised prostate cancer, intermediate risk, Localised prostate cancer, high and very high risk, Biochemical recurrence of prostate cancer, Metastatic hormone-sensitive prostate cancer, Non-metastatic castration-resistant prostate cancer, Metastatic castration-resistant prostate cancer, Neuroendocrine and small-cell prostate cancer
Showing the organ this term concerns: Prostate cancer.
The glossary entry explains the word; the readout page carries the scoring rule, the thresholds approvals use, the companion diagnostics and the tests.
It is the prospective test of the PI3K and androgen receptor feedback hypothesis in men, and it shows both halves of the answer: the biomarker-selected population benefits, and the benefit is small enough that the toxicity has to be weighed honestly.
The first randomised evidence that the order in which prostate cancer treatments are given changes how long they work, independently of which treatments they are. It is also a rare trial in which quality of life pointed one way and the primary endpoint pointed nowhere.
It splits the alterations into two groups with different practical meanings. The repair defects are present at diagnosis at close to their castration-resistant prevalence, so testing early is worthwhile; AR, TP53 and RB1 changes accumulate later, so a diagnostic sample does not answer questions about the disease in front of you at relapse.
It fills the gap between the primary-tumour atlases and the castration-resistant series by describing the disease at the moment most treatment decisions are actually made, and it identifies SPOP as a favourable marker rather than a neutral one.
It is the most disciplined outcome analysis in this disease and its result is deflationary in a useful way: most of the alterations people quote as prognostic do not survive adjustment, and the one that does, RB1, is also the one that marks the route to neuroendocrine transformation.
It gives the field a vocabulary for the states between androgen receptor-driven adenocarcinoma and small cell carcinoma, which matters because those in-between tumours are the ones most likely to be mismanaged as ordinary castration-resistant disease.
It turned a single-centre observation into a prospectively validated one and concluded that AR-V7-positive men should be offered alternatives to abiraterone and enzalutamide. It also quantified the honest limit: two assays for the same analyte disagree on nearly one sample in five.
It shows that the useful information in a castration-resistant plasma sample is in the repair genes and TP53 rather than in the androgen receptor finding that dominates the report, and it is the closest thing the field has to a head-to-head comparison of abiraterone against enzalutamide.
Shares Galeterone, Proposed morphologic classification of prostate cancer with neuroendocrine differentiation, Mutation of the androgen-receptor gene in metastatic androgen-independent prostate cancer, Nuclear-localised androgen receptor splice variant 7 in circulating tumour cells as a predictive biomarker in castration-resistant prostate cancer.
Shares ARMOR3-SV, Prostate Cancer Foundation (PCF), KEYNOTE-641, PREVAIL.
Shares PROSTVAC, PROSPECT, Prostate Cancer Foundation (PCF), SWOG 9916: docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer.
Shares PTEN protein loss and clinical outcome from castration-resistant prostate cancer treated with abiraterone acetate, COU-AA-302, ERA 223, Prostate Cancer Foundation (PCF).
Shares SWOG 9916, ARMOR3-SV, PROSELICA, PROPHECY: prospective multicentre validation of androgen receptor splice variant 7 and hormone therapy resistance in high-risk castration-resistant prostate cancer.
Shares Zibotentan, Atrasentan, ENTHUSE M1, 10TASQ10.
Shares Huggins and Hodges 1941: the effect of castration, of oestrogen and of androgen injection on serum phosphatases in metastatic carcinoma of the prostate, SWOG 9916: docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer, Abiraterone in metastatic prostate cancer without previous chemotherapy, RESTORE: bipolar androgen therapy after progression on enzalutamide in metastatic castration-resistant prostate cancer.
Shares Proposed morphologic classification of prostate cancer with neuroendocrine differentiation, Molecular profiling stratifies diverse phenotypes of treatment-refractory metastatic castration-resistant prostate cancer, Androgen receptor pathway-independent prostate cancer is sustained through FGF signalling, Combined tumour suppressor defects characterise clinically defined aggressive variant prostate cancers.