Interesting study, folks. We know physical progression of PCa (i.e., new metastases) can occur without PSA progression. This is known as a discordance. But we don't know how often it occurs or why it occurs. In these instances, our greatest fear is "therapy-induced neuroendocrine prostate cancer." But when met-advance/PSA level discordance occurs, it isn't necessarily the case - we can still have "normal" PCa. But how?
This retrospective study using 2008 - 2022 data published in June 2023 reveals a low subset of men (less than 10%) who had early docetaxel or androgen receptor axis-targeted therapy (ARAT, e.g., abiraterone and enzalutamide) may be susceptible to discordant progression.
With the incorporation of early ARAT in SOC, we may see this number rise. But it is important to remember that the phenomenon of discordant progression says nothing about the efficacy of treatment on our cancers. As I see it, right now, providers simply to be aware of our histories and this possibility so that appropriate monitoring occurs (scans versus relying on PSA level alone).
pubmed.ncbi.nlm.nih.gov/37316357/
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SeosamhM
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This is one of my fears that has been unlocked on this journey. I had triplet therapy with Docetaxel and darolutamide and my PSA declined steadily with my last two being <0.1. My MO and RO are content with just monitoring my PSA.
It was interesting in the summary how it was Docetaxel or an ARAT It would be interesting how it would turn out for men who had triplet therapy
“subset of men (less than 10%) who had early docetaxel or androgen receptor axis-targeted therapy”
This caught my attention because it looks as though I'm in discordant progression - I am getting focused radiation on Monday for a growing tumor in my shoulder. This is despite my PSA coming down after Pluvicto. Fortunately, my MO recognized this possibility several months ago and we are relying on scans as the telltale, with PSA as a secondary indicator. I suppose that the silver lining is that PCa progression with low(er) PSA does not necessarily mean neuroendocrine mutation. - Joe M.
You ask the (what may literally be) the $64,000 question and the heart of this issue as I see it. My scan history: Until 2 years ago (now 7 years in), I paid for annual NaF scans out of pocket since my original cancer manifest mostly in bone. Since coming under my current MO, his team has been able to use PSA doubling rate (even at a low PSA ...it reached 4 max) and my prognosis to request FDG PET at a clip of about every 8 months.
My next FDG PET is in a month - the justification will be for post-procedure monitoring after I get radiation for a tumor in my scapula that grew under Pluvicto treatment (!). My current PSA is 0.79.
After the discordance my MO suspected has been somewhat confirmed with this new tumor, will he be able to simply schedule future scans based on this fact? We will find out!
As I see it, this study cannot be used to tweak any specific treatment. After all, early ARAT and chemo has proven to extend time to castrate resistance.
However, the study can be used to support a monitoring program that doesn't simply use PSA levels. As westobutch123 infers, insurance companies have a resistance to what they deem to be unnecessary scans, but scans are the gold standard for identifying cancer progression.
There is about an 8% chance that a man who has had ARAT/chemo will see his cancer progress without a rise in PSA. That is small, but significant, and we can do better.
Just got my latest blood test back, my PSA is < 0.04 however my CgA has jumped from 107 to 789. I meet with a new MO next Monday. All that I’m reading suggests a tumor growth
I'm sorry jimmyc1243 - high chromogranin A is a scary thing. I'm glad to hear that you are seeing your MO soon. Since CgA is not a usual part of our testing, what led to the test? Symptoms?
Thanks for your concern. My Dr has been watching it every month, I really didn’t pay much attention to it. That is till last week when it spiked from 107 to 786
Basically Carcenoma can cause tumors that do not affect your PSA numbers. The tumors secrete a protein and that is what CgA measures. It’s interesting that less than 10% of PCa patients get this
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