Thanks SP. That's quite a bit of information to process first thing on a Monday morning. It's more than I really needed, in fact.
To the OP:
Risk group definition is tough. How about this one: If you have significant amounts of Gleason 4, or any Gleason 5 in your biopsy, you are high risk regardless of PSA. And, if so, RP may not be your best primary treatment choice.
In fact, Decipher Biopsy has a score for the likelihood your primary pattern on a whole-prostate exam would be a 4 or a 5. This obviously includes G7 (4+3), which, as we know, is Intermediate Unfavorable. If I were contemplating AS, I would give great weight to this type of predictor in a genomics test. I asked my uro if genomics testing was being increasingly adopted for evaluating AS candidacy, and he said "Absolutely."
This score isn't on the Decipher RP report, since the post-op path has already determined your definitive G score, but it is on the accompanying GRID report. My score for having a primary 4 or 5 pattern was 80% as predicted by genetics alone
-- a pretty accurate Monday-morning "forecast" for my G9 (4+5).
As I posted elsewhere, several recent studies have found favorable survival results for RP with high-grade PCa. With regard to SRT:Salvage Radiotherapy for Prostate Cancer
• RT is the only curative treatment in case of biochemical recurrence after surgery.
• Early SRT at the first sign of PSA rise granted better disease control.
• High-dose radiotherapy is well tolerated in the salvage setting.
• The duration of optimal ADT treatment depends on the amount of risk factors.
For patients experiencing biochemical recurrence in the absence of distant metastasis, salvage radiotherapy (SRT) with or without androgen deprivation therapy (ADT) is currently the only possible curative treatment option. Prostate-specific antigen (PSA) monitoring and the selected use of SRT has some advantages when compared with adjuvant radiotherapy. The most important one is avoidance of a potential overtreatment of patients who would never have disease progression, even in the presence of high-risk pathological features. The identification of a specific PSA cut-off seems to be incorrect. In patients with more adverse pathological features, early SRT administered at the very first sign of a PSA rise granted better disease control.
Dose-intensified SRT is feasible and well tolerated with no significant difference in grade 2 or more acute and late toxicity. At least 66 Gy must be given in the salvage setting. ADT has a radio-sensitising effect on the radiotherapy by inhibiting the repair of DNA double-strand breaks. The use of ADT in the salvage setting results in a better oncological outcome. Hormonal therapy is associated with a decrease in quality of life and side-effects depending on the duration of hormone therapy. The oncological benefit of hormone therapy duration depends on their clinical and pathological characteristics. 68-Ga-prostate-specific membrane antigen positron emission tomography-computed tomography is the gold standard in staging prostate cancer patients with biochemical persistence or recurrence after radical prostatectomy. The implementation of 18F-labelled PSMA tracers can provide a further improvement.
This has basically been the picture I've gotten from studies: the "trigger PSA" for SRT should be adjusted according to risk factors, but the rush to treat can result in overtreatment. Imaging can help make the call as to adding ADT or waiting.