Recurrence treatment protocol

Bob, it’s interesting that the PET didn’t show anything at a PSA of .59. I don’t know the answer. I’m guessing tht with that kind of a rapid rise, you could have micro metastasis that is producing the PSA, thus you’d be radiation the prostate bed with no benefit. But the alternative is HT alone, which likely won’t offer the possibility of a cure, just a stabilization. So I don’t kn0w the answer, it’s probably gonna be your decision on. What you feel comfortable with.

I’m not only not a doctor, but I’m not one of the more knowledgeable guys here, so wait for others to respond.

This is the test: https://www.onclive.com/web-exclusives/psmapet-agents-poised-to-advance-imaging-in-prostate-cancer

BobJS said...
Well actually the doctor said the negative scan was likely because my PSA is too low! The PSMA PET is a trial and not even covered. Sticker shock and didn't work despite glowing with Gallium 68. The challenge now is radiation without a specific target save for the whole fossa. Carpet bombing. And hormone therapy with both Casodex and Lupron. With a PSA still under one I wonder but am listening. Bob[/quote

Im facing a similar carpet bombing of the Prostate bed with Hormone Therapy. But my PSA is rising slower, and is at a lower level, .068.
I could be wrong, (and i'm sure if i am, someone will point it out) but my understanding is that the PSMA-Gallium scan will show mets 50% of the time at a psa of .2. Yours is considerably higher.

I just finished up HT and RT 3 months ago on persistent PSA after RP .there is a thread for us HT and RT guys,just put it in seach and it should come up...

This nomogram which predicts whether a recurrence after radical prostatectomy can be treated successfully with SRT could be interesting for you.
/www.mskcc.org/nomograms/prostate/salvage_radiation_therapy

Every case is different, but I also had an RP 3 years ago. My vacation from worry was shorter than yours. My first sign of PCa recurrence came 11 mos after surgery although I was getting ultrasensitive tests at UCSF so my first PSA over 0.015 was 0.031, an order of magnitude smaller than your .3 result last October. I gather you were not getting your tests done at UCSF or there would likely have been a bell going off somewhat earlier.

My RO recommended salvage radiation directed at the prostate bed although my low score on the PORTOS genetic test suggested I was not likely to benefit. To avoid masking the result, he recommended saving ADT for later. As it happened, the rise in my PSA was not affected at all by 39 sessions of radiation in early 2017. My RO concluded that the cancer throwing off PSA was not in the bed. Although this was disappointing, it at least provided some information about my cancer. I subsequently enrolled in a clinical study comparing treatment with ADT to treatment with ADT in combination with apalutamide (Erleada) or apalutamide and abiraterone acetate (Zytiga).

Before I entered the clinical study, I had a Ga68 PSMA/PET scan that turned up no hot spots so, like you, I had nothing treatable with spot radiation or further surgery. Given the failure of the radiation to the prostate bed and the absence of detectable metastases even as my PSA was climbing past .5, my RO concluded that I appeared to have micrometastases somewhere outside the prostate bed. One can only guess where or how many or what their genetic makeup may be. I get the feeling that there is still more that is unknown about my personal cancer than is known. Perhaps the medicine of ten years from now would provide better answers and that's one reason I volunteered for the clinical study. If I'm no longer a candidate for a definitive cure, then I am going to be part of the search.

You may wish to get a perspective from a medical oncologist or asking some more questions of your RO before committing to the treatment plan set forth by the RO. I know that adding a short course of ADT to the salvage radiation is very common. I've heard ADT described as enhancing the radiation by weakening the PCa cells before hitting them with radiation to kill them off. I don't know whether that is a proven fact. There are studies showing that men who receive ADT with their radiation fare better than men who receive radiation alone, but, to my mind anyway, that could be because the men who didn't get ADT with their radiation tended not to get ADT until much later. Perhaps the order in which ADT and radiation are administered makes little difference so long as they both occur fairly early. And there is a significant drawback in doing both at once: you will not know whether the cancer was in the region that was irradiated.

As a result of my RO's approach, I learned that my cancer was not in the prostate bed. If I had done both ADT and radiation at the same time, my "ride" might have led me to some illusion that the SRT may have been effective. Finding out that SRT was no use made it easier for me to risk a full year of heavy-duty androgen deprivation at an earlier stage. The range and potential severity of side effects from ADT had me spooked and I was inclined to put off ADT until later in the game. As it turned out, I wound up in the ADT + apalutamide arm of the clinical trial. I have pretty awful hot flashes as my testosterone is below 10% of normal on account of the Degarelix and what's left can't attach to my androgen receptors because of the apalutamide.

It would be interesting to hear what Tall Allen has to say about this as he has a more encyclopedic grasp of the research. Perhaps he knows of a study or studies that validate the hypothesis that the benefit from combining ADT with SRT is attributable to an interaction of the two rather than the mere additive benefit of ADT.

You mention doing your active surveillance with Dr. Carroll. He did my RP. The last time I saw him, we had reason to believe I was another Gleason 3+4 cured by the knife. Alas.

Tomson