Hi, I thought you would both find this interesting. I ran our forum board discussion and Jeff's links through ChatGPT. "Thanks for sharing the whole thread, Dave. Here’s a cohesive response pulling together the Mayo forum discussion, Jeff’s points, and the MDPI/urotoday references into one balanced interpretation:
1. What Jeff is flagging
IDC-P and cribriform: Emerging evidence links these to aggressive disease and poor outcomes. The MDPI review you linked makes that clear, but also admits the evidence base for “what to do differently” is still weak. There’s interest in adjuvant or intensified therapy, but this is not standardized or backed by large randomized trials yet .
Extraprostatic extension (pT3a): Another adverse factor, which by itself increases recurrence risk.
Decipher: Jeff is right that genomic classifiers can stratify risk further; in some analyses, a Decipher ≥0.4 correlates with higher metastasis risk if salvage is delayed .
2. Why your Mayo team (and most guidelines) still favor surveillance
Level 1 evidence: Three major RCTs (RADICALS-RT, GETUG-AFU 17, RAVES) compared adjuvant RT vs early salvage RT. Result: no survival advantage to immediate adjuvant, but more toxicity.
Guidelines (AUA/ASTRO/NCCN, EAU): Strong consensus is not to give adjuvant RT routinely, even in adverse pathology, but instead to monitor closely with ultrasensitive PSA and deliver salvage RT early if recurrence appears.
IDC-P/cribriform weren’t stratified in those RCTs. So we know these variants are bad actors, but we don’t yet have proof that treating before PSA rise changes survival.
3. Where nuance is needed (your concern is valid)
For men like you and s00nerzfan, it’s natural to feel the “standard cookie-cutter” plan may underserve aggressive biology. Jeff’s concern is rooted in real biology, but the evidence gap makes most top centers reluctant to expose every patient to RT up front.
A reasonable “middle ground” is exactly what Mayo has you on:
q3-month ultrasensitive PSA (much tighter than community follow-up).
Return visit >0.1 ng/mL — already a lower threshold than traditional 0.2.
Readiness to escalate with salvage RT ± ADT if PSA changes, with imaging layered in.
4. The role of Decipher
For low/intermediate risk, Decipher helps decide if you can avoid treatment.
In high-risk, its role is less about “if you need treatment” (you likely do if recurrence happens) and more about how soon and how intense salvage should be.
If your Decipher is high (>0.4–0.6), Mayo may shorten the leash further (e.g., act at 0.1 confirmed, add ADT with salvage RT).
5. Bottom line for you
You’re not missing the boat by not doing adjuvant therapy now. Your plan matches best evidence: heal, monitor closely, strike early if PSA rises.
IDC-P and cribriform do justify heightened vigilance — and Mayo has already lowered your PSA trigger compared to standard.
Future options: If salvage is ever needed and standard PSMA PET under-performs, you’ve got alternatives in reserve (Axumin, C-11 choline, pelvic MRI, investigational Zr-89 PSMA).
Your strategy of recovery (diet, exercise, strength) is not just quality-of-life; it’s medically smart. It makes you stronger for whatever next step may come.
👉 If you want, I can turn this into a forum reply draft that validates Jeff’s points but also reassures folks (like s00nerzfan) that the Mayo/early salvage approach is evidence-based, not complacency. Would you like me to sketch that reply in your “voice”?
FWIW: I’m a Gleason 4+5=9 pt3b with Cribriform and intraductal. I have asked my medical team for the most aggressive treatment I can have. My prostatectomy was 3 months ago, started Firmagon 2 weeks ago, Xytiga 2 weeks from now, and 39 sessions of radiation later in September. I will be on Firmagon for 3 years (unless I switch to Orgovyx) and Xytiga for 2 years. Once the radiation is done, I am going to try and persuade my MO to put me on Carboplatin or some other Chemo. I am 50 yo and trying to last 5-10 years. Let me know if you have any questions. Thanks!