Is anyone else oligometastatic with low PSA, post surgery?

According to Doctor Scholz At the latest PCRI conference SBRT is the way to go just zap it.

Yes, your doctor is probably going to do salvage radiation, It is the standard of care once your PSA hits .2. You can wait till that happens. Get those spots zapped and see what happens with your PSA.

ADT would make sense to Reduce the likelihood of a reoccurrence.

Of course you don’t say what your Gleason score is or maybe a decipher score. Something to give an idea of how Aggressive, your cancer is. A lot of the decision-making about your cancer treatment is dependent on that Gleason score.

I'm low risk on almost every metric. Gleason Group 2, T1, the MSK nomogram gives a 2% likelihood of me being recurrent due to risk factors. Genetics is clean. No Decipher though.
There was PNI and cribiform on my biopsy. Clear margins, small contained lesion in a small gland. 3.7 PSA was my max. 2.9 at surgery. It has decreased the last 2 tests.
Thinking of doing whack a mole without ADT and seeing how that goes.

I'm just wondering if there is anyone else out there who has experienced this choice. I know I'm a rare case, and I wonder how others have decided on what they chose.

When I was 51 years old, my PSA peaked at 2.0 right before surgery (Dec-17). I was Gleason 4+3=7. In early 2019, I had the prostate bed radiated with 2 years of ADT (PSA was under .2 when I started ADT). Then in early 2023, my PSA rose to about 1.5 within 6 months before radiating a lymph node region. I am about to start triple therapy treatment due a reoccurrence on the hip bone, along with a few smaller potential legions growing in size when PET scans are compared over the past few years. My PSA hit .25 this year before I went back on ADT. One of the reasons for the triple therapy is because I have had low PSA scores, so my oncologist believes these smaller lesions are going to be a bigger problem than my PSA score suggests. She also thinks that based on my age (58) that we should hit it hard for the best long-term outcome.

Mayo tells me 10-20% of advanced cases are in men with no or low PSA. Separately, I was told by Mayo to start ADT at least 30 days before radiation with 18 months being the longest needed duration (when radiating the prostate bed and the lymph node region). When I was contemplating hip radiation, Mayo was going to put me on ADT for 4 months (start ADT 30 or more days before radiation, which was going to be done in a single session). But anytime I talk to anyone about radiation, so ADT has been included.

I'm still looking, but I haven't found any literature yet about cases of regular advanced prostate cancer progressing without expressing PSA on the ultrasensitive test (< 0.01).

I've seen a couple about progression when PSA was < 0.5 (the lowest early tests could detect), and a fair number when PSA was detectable in the low range (< 5.0).

That's one reason they often use uPSA to give early warning of recurrence for metastatic prostate cancer.

Note that there's a different, rarer type of prostate cancer, neuroendocrine, that does not express PSA as it spreads, but the adenocarcinoma that most of us have does.

There is a lot of literature about the fact that even though PSA is undetectable metastasis can occur.

NIH and Scirntificliterature said the following

A patient with Gleason 10 adenocarcinoma achieved undetectable PSA after radiotherapy and androgen deprivation therapy (ADT) but developed spinal cord compression and liver metastases within six months. Biopsy confirmed poorly differentiated carcinoma of prostatic origin, highlighting the disconnect between PSA and tumor burden

Prostate cancer progression and metastasis can occur even when prostate-specific antigen (PSA) levels are undetectable or extremely low, particularly in aggressive or atypical tumor subtypes. This phenomenon, though rare, is documented in multiple clinical studies and case reports. Below are the key findings and implications:

In a study of 46 patients with metastatic prostate cancer, 10 patients (22%) developed metastases despite undetectable PSA levels (< 0.1 ng/mL). Eight of these cases involved small cell carcinoma, an aggressive histologic variant.
• High-risk features were common:
• 85% had Gleason scores ≥7
• 63% had locally advanced tumors (T3/T4)
• 46% exhibited atypical histology (e.g., ductal, sarcomatoid, or small cell).

Thanks, Jeff. That is very useful information.

For others reading, note that all of the cases Jeff mentioned were based on the regular PSA test (< 0.1), not the newer ultrasensitive PSA test (< 0.01) — probably because uPSA wasn't widely available yet when they were collecting the initial data — and also that 8/10 of the cases involved involved small cell carcinoma (the "neurodendocrine cancer" that I mentioned in my post), rather than the more-common adenocarcinoma.

So for the vast majority of us, especially those being monitored with uPSA, as far as I know there's no evidence ... yet ... that progression without a corresponding PSA rise is a significant risk. I'll keep watching developments.

Thanks. That sounds like a lot to endure. I'm just starting out with recurrence after surgery, trying to figure out if the bone lesions are real and what to do about them.

If you want to see if they are real PCa metastases, do SBRT first without ADT. If your PSA falls then you know positively that they were PCa.
You could then institute ADT, depending on what your oncologist thinks…probably ‘yes’. If they do not respond at all and PSA stays the same or rises, then you have the more generalized bed/node scenario and SRT could then be initiated with ADT.
Phil

Thanks. That id exactly what we just discussed today. I have one more opinion at UCSF, but it seems we are, finally, converging on a plan!

Similar case: a ‘low’ 0.36 PSA, 17 yrs post RARP, and PSMA Pet shows metastasis to lung. So, similar with lower PSA being expressed with metastasis.

We have not been offered SBRT. We asked and the notion was to get going with ADT and chemo fearing some odd mutation that isn’t showing itself. From what I’ve read SBRT sounds like a good option with less collateral damage and ablation is another treatment that we may consider if there are residual spots after this chemo hit (again, need to talk with team about it).

As for salvage radiation, it was offered before we had the PET scan, as a ‘standard post surgery tx’ when PSA creeps up. We pushed for imaging and glad we avoided radiating the prostate bed because nothing showed up there on MRI or PET. Are there ca ‘seeds’ or stem cells unseen somewhere? Probably, but we are now learning that chemo and radiation may get the dividing cells, but not the stem cells, as prostate cancer cells are heterogenous. Those buggers are the ones that ‘come back’ or become resistant and the ones that need an attack still tbd, it seems. That’s why this has become like a chronic illness and long term battle. This is just my view from a lot of reading, others may agree or disagree.

Anyway, whack a mole with SBRT seems a promising option to consider and avoiding random radiation to areas without confirming tumor presence sounds like something to dig into with more questions.

Good luck and keep us posted. We low PSA with Mets are in a special group. Others here with Cribiform can tell you more about that. Our surgery pathology was 2008 and they did not look for that at the time, although we did have PNI (another interesting rabbit hole).

Wow, sorry, I carried on …