1st LapCorp PSA .019 CRAP!

For past seven years my uPSA is holding very low stable 0.03X range, no ADT. (Post RP, salvage RT to prostate bed, salvage extended pelvic lymph node surgery, one-year bicalutamide).

Although it would be wonderful I do not attribute my lingering uPSA to other glands nor benign healthy prostate cancer cells. (How could these 'left behind' cells survive for nine years?).

Ten yeas ago my first biopsy pathology opinion was 3+3 and even back then there was much talk this is not cancer. (Turned out I was 4+3). I find this current web article and referenced links interesting: https://sperlingprostatecenter.com/gleason-6-prostate-cancer-progress/

humm, any research or collegiate text to share on this?

Dalota if you are asking me no I make no such suggestions. I do believe we face many disparities with this beast. Given the rising death rate, given number of men on ADT is also rising, and the fact that men indeed have cancer spread after 10+ years, IMO still much is not understood.

If remaining and thriving benign residual glandular tissue is not uncommon after nerve-sparing prostate surgeries, why is there not a lot written on this?

Sharing an interesting parallel read.
https://www.mskcc.org/news/new-discovery-explains-how-prostate-gland-regenerates-itself

The key point still seems to be to have "same as possible" tests done repetitively over a period of time--the sweet spot seems to be at 3 month intervals--and then make a judgement about what is happening.

Two tests a few weeks apart don't tell us anything other than show us the between-test variability (statistical margin of error). And, this would apply whether the patient is 3 months or 10 years post-treatment. That being said, the longer the span between treatment and unexplained PSA rise, the less likely it is going to be seriously ugly.

Hi All, I just got back from my appt. with a new oncologist at Ohio State University. Here is what I was told.

They did not feel I was having BCR. Thy ran a PSA test before my appt. and I had the results in my phone in 10 minutes. This what they do with every so they can talk about it during the appt. The test was in my phone before I went into see the Dr. Their lower limit is .04 and my PSA with them today came back at <.04 Not surprising from last week. They do not believe in the ultra sensitive PSA......BCR to them is determined on a case by case basis and always involves a consistently rising PSA of large amounts. They would never pull the trigger on SRT below .1 They even mentioned they see patients bouncing around .07-.08-.09 and as high as .11 The doctor said and I quote "we have some patients that have been doing this for decades."

They were very confident I would never need SRT....ha....however, I should continue doing PSA. They told me to go back to annual PSA....and if I freaked call them anytime and they will let me test. SRT with HT in GG1 and GG2 cases is very successful for them and they feel it is a good second shot a cure. It is much better than it used to be.

As for the detectable PSA I am having....without saying a word they said in their experience it is left over tissue as they have seen other patients PSA bounce around for decades and never have BCR....Since I am so far out from surgery in 2008 and this is my first ever uPSA they said it could have been there for years....they do see it happen frequently....

I am going to digest this for a while but I am OK for now with the <.04 as I was always <.03 anyway and they said with GG1 and GG2 nobody would be doing SRT below .04 no matter what....if they are they shouldn't be.

Ohio State is a teaching/research hosiptal.....so they see a few cases I am sure....

I'm going to go with it for now.

16 years and undetectable....

Dakota, The stated Objective of the article you cite is to see “if benign glandular tissue (at the surgical margin (BGM)) increases the risk of biochemical recurrence.” (not measurable (misleading) PSA). I added this 2014 article to my library when I was evaluating my RP nadir of uPSA 0.051. Although this is a limited space to ‘discuss’, trying:

I did not find this statement in COMMENT section most interesting: “The most interesting finding of this study is the identification of BGM after both ORP and RALRP was not associated with recurrence, either biochemical or clinical, during a median follow-up interval of 49 months after ORP and 28 months after RALRP.

What I found most interesting this this: the explained method for determining the presence of remaining tissue was review of surgical tissue by a single uropathologist and that regression analysis was utilized to examine associations of benign glandular tissue with surgical approach and biochemical recurrence. Another way to say this - one (smart) person estimated.

Another interesting detail: “It is important to note the follow-up for those with BGM is relatively short, and sufficient time for cellular proliferation and resultant increase in serum PSA may not have elapsed. Extending followup further should clarify whether BGM leads to low, detectable levels of PSA that may not meet threshold for defining biochemical failure.”

Nowhere in this research or others I have in my library suggest BGM is producing measurable PSA many years after surgery.

A similar Conclusion from this 2021 article:
“The presence of BGM at RP was not associated with increased risk of MSM, detectable PSA, BCR or progression after detectable PSA.”
https://www.auajournals.org/doi/10.1097/JU.0000000000001793

ChrisR, a good discussion - this topic has been my focus for nine years. Because you are thinking all this over – a further share (again not promoting a position – simply sharing my experiences. I am thinking to stop here ;)

I have consulted with a number of docs who do not believe in the ultra sensitive PSA tests and question my self-directed testing efforts. When I show them my nine years of graphs and tables their expressions speak volumes. As I have experienced low detectable bounce for nearly seven years now, I would be asking about cancer stem cells and senescent cells knowing that men do realize a dangerous cancer 10, 15+ years later; if something else does not take their life first - as is the case for most men with prostate cancer. Regarding patients bouncing around .07-.08-.09 and as high as .11 and for decades: Really, ‘decades’ is 20+ years – really?

My post RP nadir was 0.051 and indeed was cancer – how can it not be cancer at 0.04 and lower? As I share I had six cancerous pelvic lymph nodes confirmed by third treatment, salvage extended pelvic lymph node dissection, at 0.113. This was after rise from my post salvage RT nadir of 0.075. A number of docs have said to me 'I have never seen a patient with multiple cancerous pelvic nodes at 0.13'. I then ask them, how many of your patients have had salvage extended pelvic lymph node surgery? The answer is always the same – “none’"

I always find it curious when a doc says something like “they were very confident I would never need SRT but keep testing. As for “SRT with HT in GG1 and GG2 cases beging very successful, since my RP my intent continues to be doing all I can do defer need for ADT; thereby deferring the likely reality of CR for as long as possible.

As discussed with Dalota, I would also be asking for the provable science that left-over tissue is the cause. Would this not take a biopsy? I am not aware of a single case of a biopsy proving the presence of sufficient lingering healthy tissue (and no cancer) to be source of low detectable PSA (I have asked this of docs in Europe too, where I went for imaging that is not available in US and for salvage ePLND that was not readily available to me in US).

They have seen a lot. I would listen to them and not be influenced by what you read here by people who are not physicians.

Nano

I appreciate your passion and deep engagement with this topic, as well as your willingness to share your unique journey and experiences. That said, I think it’s important to keep the diversity of clinical perspectives and individual patient cases in mind. Just because something hasn’t been explicitly proven or is outside the realm of your specific experience doesn’t mean it doesn’t happen or lacks validity. Let me address a few of your points.

First, regarding the idea of patients bouncing around PSA levels like 0.07–0.11 ng/mL for decades, yes, “decades” might be a term that raises eyebrows at first glance, but it’s not unrealistic when considering stable, low-level PSA patterns, particularly in men more than 10–15 years post-RP. At such low PSA levels, benign sources of PSA—such as residual benign tissue left behind despite negative margins—are a plausible explanation. While a biopsy of this tissue isn’t typically done (because it’s invasive and unnecessary in most cases), the phenomenon is widely acknowledged in the medical community, and there’s plenty of anecdotal evidence from experienced clinicians who have monitored patients in this category.

Second, you mentioned that your post-RP nadir of 0.051 was cancer because you had subsequent progression. While that was your specific case, it doesn’t mean that every measurable PSA at these levels represents cancer. For example, someone without evidence of progression 10–15 years after RP (and with a Gleason Grade Group 1–2 tumor) could very likely have residual benign prostate tissue as the source of low-level PSA. It’s dangerous to generalize from one individual’s case, no matter how carefully documented.

As for your skepticism about the science behind lingering benign tissue contributing to low PSA levels: While a biopsy is rarely done, studies have shown that benign prostate cells can persist in periurethral tissue and other regions near the surgical site despite negative margins. These cells can produce detectable PSA in the absence of cancer, especially with ultrasensitive testing. Imaging or biopsies aren’t typically pursued in such cases because they wouldn’t change management unless the PSA was rising rapidly or reaching concerning thresholds.

Finally, I respect the unique challenges you’ve faced with your lymph node involvement and your focus on delaying ADT. However, the rarity of your situation shouldn’t invalidate other patients’ experiences or the clinical decisions of doctors managing stable, low PSA rises over long periods. The prostate oncologist at Ohio State, for example, is reflecting a very reasonable and evidence-based approach when monitoring stable, low-level PSA fluctuations without rushing into unnecessary treatments.

In short, while your experience is valuable, it’s not universally applicable, and there’s room for multiple clinical approaches to similar PSA scenarios. I think we should all strive to encourage nuanced discussions without dismissing the experiences or opinions of others outright.

Chris - you make an excellent point. If in fact it’s PCa cells it had to escape before your prostate surgery more than 16 years ago but more like 20. Your Psa would have very different kinetics and would be rising much more rapidly which is the exact point my urologist made to me. You absolutely have nothing to worry about. I’m not exactly sure what Nano is trying to do but he should reconsider making some of his comments before posting.

Hi Chris, answering your questions, my post RP pathology was G4+3 (initial path opinion was 3+3 which was upgraded to 3+4 on 2nd and 3rd opinions). Taken lymph nodes were clear. One section indicated 'involved margin'.

The imaging I commented on was done in January 2018 at Radboud UMC, Nijmegen, Netherlands. These included common bone and CT scans plus Ga68 PSMA PET CT and Ferrotran nano-particle MRI. These all done at PSA 0.131. The 'common scans' and the Ga68 PSMA were clear while the Ferrotran successfully identified five suspicious pelvic lymph nodes. Note the Ga68 PSMA PET was in limited trials in the US at that time - I applied but was declined participation.

I do hope in some way my comments help you reach the answers/decisions your seem to be searching for.

Post Edited (NanoMRI) : 1/23/2025 12:49:47 PM (GMT-5)

All good Chris, yes emotions can be very high and challenging, not only because this is cancer, we face so many disparities.

Although I have no certain answers for my very low stable uPSA for past seven years I will take it for years to come. Thing is, there are credible (yes maybe theoretical) explanations such as cancer stem cells, senescent cells, micromets, which is why I continue to keep very close watch. And of course I had cancer confirmed in pelvic lymph nodes.

Add all the data indicating the death rate is rising, as is the number of men on ADT and facing CR, and what a challenge we all face. Without question the health care industry is well on its way to treating this disease as a chronic illness with ADT – the exact opposite of my approach. A podcast promotion in my ad feed is titled “The Evolving Role of Hormone Therapy in the Management of Prostate Cancer”.

Side-note, I have read Dalota’s comments, not favorable really, perhaps a bit snide, so far not responding as IMO the focus should be your original post.

All the best!