Hi- I thought I would seek some advice before I meet with my MO tomorrow morning. I have responded well to treatment of metPC since my dx 11+ years ago. About 2+ years ago my PSA became measurable and was rising. After about a year or so I think it reached .37.
Following a PSMA scan, my MO saw only my largest tumor growing and suggested we radiate it and continue with Lupron and Abiraterone. That seems to have worked for a short as my PSA became immeasurable once again.
However- over the last 15-18 months, my PSA has been rising form:
<.05, .05, .06, .06, .09 and then yesterday it was measured at .14.
I assume my MO will have me PSMA scanned again, when she thinks the test becomes worthwhile based upon my PSA score.
My questions: Dr Kwon, from his video on Youtube seems to indicate that those of us on ADT for a long time can possibly have tumors growing without ANY rise in PSA. Should I get a PSA immediately or should I wait.
Also- should I add docetaxel to my treatment now, or should I wait? Also- should I try switching from Prednisone to Dexamethasone ?
I guess more radiation is an outside possibility but I think that train has already run as I am getting hip replacement surgery on Wednesday because the 2 previous times my hip was radiated caused necrosis (lack of blood flow). So- I doubt the hip can be radiated again and my other tumors are located on my vertebrae and I possibly my ribs.
Any other thoughts or suggestions are welcome.
Thanks to all
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jfoesq
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When Lupron and Zytiga started to fail I enrolled by chance in a trail at Dana Farber with LuPSMA177. That was 2022. I completed all 6 cycles. Initial response was excellent but not durable. PSA started climbing. I met with Sam Denmeade Jan. 2023. He said I would be an excellent candidate for BAT. I was unable to find an MO that would assist so I set forth on my own with the help of others already utilizing this therapy. The big difference is I am using Propionate which has a short half life, and to some, think it shocks the cancer because of this. Only a theory. Well I was indeed a responder and obtained a 50% reduction in PSA. With this information my local MO decided to assist me. In fact he is employing BAT with a few of his patients. At least one with positive results he has shared with me. Once again he is using Cypionate with a longer half life, slower decay.
I did Lupron and Zytiga for about 18 months. PSA started to rise. That's when I contacted Dana Farber for the LuPSMA177 trial. Why you ask. Personal decision. I tried SOC for 15 years and I felt the need to look outside the box. BAT has greatly improved QOL as well. My approach now is to attempt to maintain or somewhat control my cancer. No longer searching for the silver bullet.
My initial response to BAT was very positive. The first 6 months. It fluctuated a bit after that but doing rBAT now with stable PSA. Back in October I had SBRT on L3. So between Testosterone and Nubeqa things are stable.
Before changing treatments you need to have evidence of radiographic progression of the cancer. Most people recommend to do a PSMA PET/CT with a PSA around 0.5 or higher.
tango65- I am familiar with the PSMA at .5 or higher but based on what Dr. Kwon said about progression being possible for those who have been on ADT for a while even when their PSA is undetectable, I wonder why that measurement is used.
The .5 is used because I believe the scan can only see collections of cells greater than 10,000,000 (off the top of my head)
Even cancer cells that produce almost no PSA, produce a tiny bit of PSA. The research around the newer pet scans informs psa cutoffs. It’s unlikely to see anything on a scan below a certain PSA level. Insurance tends to reimburse expensive tests when they are likely to produce useful/ actionable information. Another reason for psa thresholds that feel somewhat arbitrary.
AI May one day soon be able To compare x00,000,000 scans and predict which ones have malignant changes earlier.
I am confused. Dr. Kwon seems to state that ADT can sometimes permit the cancer to spread/grow WITHOUT an increase in PSA and even when PSA is immeasurable. The only way I think he can state that is in the basis of scans. Which means scans he has performed on SOME individuals without a measurable PSA are, in fact, showing changes (growth) of the cancer. This sounds to be unusual but does seem to occur. What am I missing?
Pet scans are more likely to observe metastatic sites above a certain level of PSA. That statement is based on clinical studies and data.
And, the way that I understand it, prostate cancer cells can evolve in a way that causes them to 1) not require testosterone for proliferation 2) produce much less psa than androgen sensitive lines of cancer cells.
This can mean that a person with cancer which has evolved towards androgen independence, can have increasing cancer activity on a scan, while still having negligible psa. PSA becomes a less reliable indicator of progression than scans, when cancer becomes androgen independent.
Kwon scans irrespective of psa level and is able to compare scans to determine whether or not there is anything brewing in his patients.
That’s what I thought. Not sure why people say the scan is ineffective with PSA less than .5. Sounds to me like it can be effective at .01 or less. I guess the issue is insurance companies and the low percentage of times that it’s meaningful at those lower levels
The issue is almost always the insurance companies.
If your doubling time is moving towards exponential, you will be at .05 shortly. I’d also like to add, based on your history with PC, you are alive more than 10 years later, and that bodes well for continuing to stay alive. And when the most established tool for pc (HT) no longer keeps psa undetectable, it’s hard not to feel anxious.
I also don’t think it will change the treatment path, waiting to .05. But what I think is based on opinions/ experiences of non DR, in the cheap seats. Don’t listen to me.
I'll weigh in on this, jfoesq. The direct answer is yes, we've known since the 2000s that "progression of prostate cancer can sometimes occur in the presence of an undetectable or low serum PSA level" (see 2010 Reference 1 below). This paper referenced an earlier 2007 study (see Reference 2) and continued to say that "(t)hose patients with metastatic prostate cancer and a low serum level of PSA account for less than 1% of all patients with metastatic prostate cancer." It should be of note that these discussions are NOT about neuroendocrine PCa, which is that related mutated beast that we all fear.
Summary: PCa can progress with very low PSA, but it is extremely rare. Reference 2 concluded that "(c)omplete physical evaluation and imaging studies may be indicated in the surveillance of patients with high-grade, locally advanced tumors, especially when atypical histologic variants are present." This seems to be supported by another 2022 case study review (See Reference 3).
So, you have some talking points with your MO. Does your case involve "atypical histologic variants" as indicated by original biopsy? Has any information been gathered to confirm/deny progression into "atypical", like genomic testing?
In my opinion:
You are being appropriately vigilant, but jumping data to treatment options is not yet warranted - ADT+Abiraterone has definitely been your buddy so far! Before you change therapies or even approaches to therapies (like switching up corticosteroids), get as much basic information as you can that can inform your decisions.
If you want to "do" something while you are getting this data, I suggest looking into Provenge - immunotherapy that statistically extends lives with absolutely no other intermediate metric to track its effectiveness! I say that tongue-in-cheek, because I got it, and would do it again, by golly!
Update: Just finished my consult with my MO. She confirmed what her colleague Dr. Kwon indicated (that cancer can spread even with an immeasurablePSA) but said that happens only about 5% of the time when the cancer becomes neuroendocrine AND that other blood tests, such as alkaline phosphate and liver tests among others would offer clues that such an event might be taking place- and- since all my other labs are normal- she thinks it best for me to wait til my PSA hits 2.0 before deciding how to proceed. She said depending upon what the scans reveal at that time, would impact the next step she would recommend we take and can’t simply state what step(s) that would be at present. Having said that, she did indicate that switching from Prednisone to Dexamethasone would probably not be her recommendation for 2 reasons: a) how it works remains unknown; b) I am having my hip replaced in Wednesday BECAUSE of necrosis and using DEX is thus not a good idea
I think my MO, Dr. Dana Rathkoph from MSKCC in NY is very knowledgeable and I will continue to follow her advice- at least for the time being.
I am still happy to hear any thoughts or ideas from any of you, as long as they have a scientific basis.
Typo: Apologies- I mistakenly wrote 2.0 when I meant to write .20. To clarify- my MO intends to do a PSMA when my PSA reaches .20, which I assume will be in the next 3-6 months
Very well- thx. Played Pickleball 5 weeks after (which was too soon, but I got away with it) and started playing regularly after 7. Just played about the last 8 out of 10 days and am not even aware of my hip- I am only aware of my age and wish I still had my testosterone.
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