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In cancer that has already spread, this is the time until the scans show it getting worse, or the man dies. It deliberately ignores a rising PSA on its own, because in prostate cancer the PSA can rise for reasons that do not mean the treatment has stopped working.
Radiographic progression-free survival is the time from randomisation to the first documented progression on imaging, or death from any cause, whichever comes first, with prostate-specific antigen rise alone explicitly excluded as an event. It is the workhorse endpoint of metastatic castration-resistant prostate cancer trials, and the reason it exists is the Prostate Cancer Clinical Trials Working Group's judgement that biochemical progression is an unreliable proxy in a disease where androgen receptor-directed drugs can move the PSA independently of tumour burden.
The imaging rules come from PCWG2 and are carried forward by PCWG3. Soft-tissue disease is assessed by RECIST. Bone disease is assessed on bone scan, where progression requires a minimum of two new lesions; PCWG2 advises against a follow-up bone scan before 12 weeks of treatment unless clinically indicated, because of the flare phenomenon, in which a responding bone metastasis looks worse before it looks better; and confirmation requires a further scan performed six or more weeks later showing additional new lesions. That is the rule usually shorthanded as two plus two. PCWG3 added time to symptomatic skeletal events and the concept of no longer clinically benefiting, to separate the first evidence of progression from the clinical need to change treatment, and asked that progression in existing lesions be documented separately from the appearance of new ones.
As with metastasis-free survival, the operational definition is set by each protocol, and three things vary: the imaging schedule, whether the reads are by investigator or by blinded independent central review, and whether bone-scan progression alone is enough. That is why reported medians are not interchangeable. COU-AA-302 reported radiographic progression-free survival of 16.5 months with abiraterone and prednisone against 8.3 months with prednisone alone in 1,088 chemotherapy-naive men (hazard ratio 0.53; 95 percent confidence interval 0.45 to 0.62). TRITON3 reported imaging-based progression-free survival of 11.2 against 6.4 months in its BRCA subgroup. Both are radiographic progression endpoints; neither was measured the same way.
Showing the technology this term belongs to: PSMA PET.
The randomised proof for PARP inhibition in BRCA-altered prostate cancer, and the clearest evidence that the homologous recombination repair gene list should not be used as a single yes-or-no test. ATM-altered disease needs a different answer, and does not yet have one.
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.
The first predictive resistance biomarker in prostate cancer, and a mechanism rather than a correlation: a receptor with no ligand-binding domain cannot be blocked by a drug that binds the ligand-binding domain. It is also the origin of the case for androgen receptor degraders, which destroy the protein rather than blocking a site the protein no longer has.
The trial that made an androgen receptor inhibitor the usual first treatment for castration-resistant prostate cancer, and that delayed chemotherapy by a long margin for most men. Its effect sizes are why later trials in this setting are judged against a hazard ratio near 0.7 for survival.
One of the most cited trial reports Europe PMC returns for Abiraterone acetate in Prostate cancer, so it is a natural first reading for anyone weighing the idea it is linked from. The record was linked automatically by title and abstract; read the abstract above and the paper itself before relying on any figure.
An oral drug that works after chemotherapy has failed, in a disease where the previous option was more chemotherapy. Together with abiraterone it moved castration-resistant prostate cancer from a chemotherapy disease to a hormonal one, and set up the sequencing questions the field is still arguing about.
Shares PSA50 / PSA90 response, TRANSFORMER: bipolar androgen therapy versus enzalutamide in asymptomatic metastatic castration-resistant prostate cancer, Randomise the order of treatment, not only the drugs: a strategy platform for metastatic prostate cancer, Castration-resistant prostate cancer (CRPC) and the tags gu, prostate-glossary.
Shares AR-V7 and resistance to enzalutamide and abiraterone in prostate cancer, Neuroendocrine and small-cell prostate cancer, PSA (prostate-specific antigen), Castration-resistant prostate cancer (CRPC) and the tags gu, prostate-glossary.
Shares TRITON3: rucaparib or physician's choice in metastatic castration-resistant prostate cancer, Metastatic hormone-sensitive prostate cancer, Regulatory divergence between regions, Acquired resistance to every therapy and the tags gu, prostate-glossary.
Shares PSA (prostate-specific antigen), Hazard ratio (HR), Metastatic hormone-sensitive prostate cancer, Trial design, endpoints and cost and the tags gu, prostate-glossary.
Shares PSA (prostate-specific antigen), Hazard ratio (HR), Trial design, endpoints and cost, Prostate cancer and the tags gu, prostate-glossary.
Shares PSA (prostate-specific antigen), Trial design, endpoints and cost, Prostate cancer and the tags gu, prostate-glossary.
Shares Hazard ratio (HR), Metastatic hormone-sensitive prostate cancer, Prostate cancer and the tags gu, prostate-glossary.
Shares Metastatic castration-resistant prostate cancer, Prostate cancer and the tags gu, prostate-glossary.