Back on 1/8/19 I had an Axumin scan to try to locate the area of recurrence. That test found no evidence of metastatic PCa. I then applied to the following clinical study (Yale location):
NCT03739684, PyL 3301, Study of 18F-DCFPyL PET/CT Imaging in Patients With Suspected Recurrence of Prostate Cancer clinicaltrials.gov/ct2/show...
The people at Yale were amazing - they go the ball rolling very fast and I was scanned last Thursday 1/24/19. .
This afternoon they called with the results:
- They found the cancer in several lymph nodes:
The largest is about 11mm and is located in the right pelvic area.
He mentioned 3 to 5 smaller spots in lymph nodes around the lower spine.
Nothing noted in the bones.
- They said that Yale's approach at this point would be to start ADT with Zytiga & Prednisone and referenced the CHAARTED and STAMPEDE studies.
I have an appointment with my urologist tomorrow and will be moving forward with the ADT while I await input from my MO on the Zytiga & Prednisone part of the treatment.
Yale will also be sending the film of the scan for my RO to review. Systemic treatment is a given at this point but I'd also consider treating the lymph nodes, or at least the largest one, if safe and potentially beneficial.
Gene
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shueswim
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I am struggling with the question of why treating any LN at all and expose the body to more radiation at this setting? Is there any long term survival?
TA, I am in same situation but has not done the 18F pet scan yet and am considering SERIOUSLY of skipping these tests and try to chase the cancer and find where it is and go direct ADT. Your thoughts would be greatly appreciated.
You're not exactly in the same situation. Shueswim went into his PET scan with a PSA of 1.5 and found that all his detectable mets were in is pelvic LNs. The advantage of whole pelvic radiation after there are known pelvic LN mets is discussed here:
Presumably, the advantage Touijer found would still obtain after the prostate bed has been treated.
In your case, your last PSA was lower (0.5) so there is less chance anything will show up on a PET scan. Who knows where the cancer went next? Recently RTOG 0534 showed that whole pelvic salvage radiation conferred a survival advantage over prostate bed only, and presumably pelvic LN would still be beneficial after the prostate bed has had SRT.
So the risk you're taking by treating the pelvic LNs now is that the cancer hasn't travelled there. And the risk you're taking by waiting until a PET scan might show something is that you're giving the metastases more time to flourish.
Sometimes PET scans will pick up mets when the PSADT is rapid. DCFPyL is the most sensitive and specific of the experimental PET scans.
Thank you for your pcnrv blogspots on this complex topic, you have a real gift for synthesising information from multiple studies into digestible form.
You say that PET scans sometimes pick up Mets when PSADT is short, and I see lots of papers that talk about the kinetics of recurrent PSA, but very few that really nail PSADT down, particularly at low PSAs.
Beyond the fairly obvious “shorter PSADT = more aggressive disease”, are you aware of any work that has tried to explain this observation in terms of the underlying cellular or genetic landscape, or tie it to any particular therapeutic approach?
My PSADT post RRP has stuck at about 3.7 months and perhaps correlates with several Decipher GRID readings for aggressive growth - but so what am I to do with that??
I suspect there’s just too many variables and too many other things going on for PSADT to have received a lot of attention, but it always seems to get tossed in as an important variable without anyone being too specific?
Thank you again for your dedication in this area, which I am sure assists many of us greatly.
Thanks for your kind words. When PSA was first discovered and characterized in the 1970s, it was proposed as a biomarker because it closely correlated with metastases. While it was found on every prostate cell, but it only leaked into the serum when the cells were disrupted mechanically or by the leaky vascularization around tumors. In general, micrometastases and "dormant" tumors put out less PSA; larger, rapidly growing and more widespread tumors put out more PSA (owing to their greater vascularization).
There have been many trials of vascularization inhibitors, but they have not been shown to have much benefit so far. Metastasis-directed therapy shrinks the larger tumors, which certainly reduces serum PSA, but whether that translates into any net benefit in terms of radiographic progression or survival is yet to be determined. Treating PSA is not the same as treating the cancer.
The one thing we know works against the cancer AND the PSA is ADT. Your rapid PSADT is a clear indication to begin ADT. ADT + SRT improves survival better than ADT alone. I don't really understand why you don't know what to do about it.
There have been many studies about PSADT in the recurrent setting. It is a well-established biomarker for metastasis and survival. Here are some:
Ahk1 - I understand your struggle. For me there are a few considerations that motivate my course of action. One - I’m relatively young and in otherwise great health (hows that for an oxymoron?). Two - following the play book puts me on a course for a 3 to 5 year survival. So while there is a known radiation risk for unknown potential therapeutic benefit, I made the decision to pursue the scan. It’s still to be determined if it yields another treatment option that I can combine with the systemic approach. At this point I’m willing to turn over all stones even though I know there may only be worms under them.
So, after a very successful surgery in Mar 2024, GS 8, T2CNoMx, negative margins, ECE and seminal vesicles, only 10% prostate involvement I had BCR 18 months later, SRT I started in Mar 16 failed when 90 days after the 39 IMRT treatments, my PSA was .7 then a month later 1.0.
With PSADT and PSAV less than three months a C11 Choline Scan at Mayo in Jan 17 showed four pelvic lymph nodes with PCa. Dr. Kwon and I agree on a treatment plan, six cycles of taxotere, 24 months of ADT and 25 radiation treatments.
My RO, the same one who did the SRT was able to build a treatment plan that included boosts to the four lymph nodes along with wider margins around them.
I finished treatment in May 18, labs and consult every 90 days since.
PSA went from 4.8 in Jan 17 to .8 with first treatment, less than .1 after that, T stayed at less than 3 throughout treatment.
Some lessons learned.
Data was emerging at the time of my SRT about adding ADT. My RO said there wasn’t long term data to support it, I let her talk me out of it...last time I let my medical team overrule me. To her credit, she learned from that and subsequently opened up to more aggressive treatments. She and I talked about looking through the lens of a five year window vice 10-15, can this treatment get me through the next 3-5 years, if so, ok, new imaging and treatments will come along after that.
Imaging is key in builds better radiation treatment plan, think dumb versus smart bombs....
Imaging is key (did I say that), had we combined SRT with standard pelvic lymph node radiation treatment fields it would not have included 2 of the 4 sites identified in my C11 Choline Scan.
Aggressive PCa requires aggressive treatments that combine and bring treatments forward early in the PCa. Linear and sequential treatments are destined to fail.
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New Developments in My Husband's PCA Journey
Starting Abiraterone and predniSONE
PSMA scan results 
Axumin PET Scan Results
Father’s MO now recommending adding Zytiga
