Asking advice and thoughts on my situation. I'm 5 years post IMRT to prostate and pelvic LN in 2015. Original PCa diagnosis in 2012 with Gleason 9 (4+5), Stage 4 ('locally advanced', no mets). Three cycles of ADT (4-6 months each) from 2012-2016.
From Aug 2019 to Aug 2020 PSA went from 0.15 to 2.42. In Oct. had an Axumin scan that showed no mets to soft tissue or bone, followed by two different circulating tumor cell tests to check for micrometastasis (Foundation One Liquid CDx and Biocept). Neither found any CTCs.
With no sign of mets I'm not sure what to make of the PSA increase.
[I'm on the Care Oncology protocol (Metformin, Atorvastatin, Mebendazole, Doxycycline), plus Modified Citrus Pectin, 81mg aspirin, and other supplements to inhibit angiogenesis and promote apoptosis.]
Your thoughts?
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novatimo
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Why did you start and stop and start adjuvant ADT? - that selects for resistant strains. At least 18 month continuous is needed to kill off the remainder. Too late now. You might try a PSMA scan, or just go on enhanced ADT. CTCs have high false negatives.
Had a PSMA in Berlin in 2018. No mets found. Since PSMA not yet FDA approved in U.S. my insurance won't pay for it and I can't afford it. Believe I'm eligible for this PSMA clinical trial (clinicaltrials.gov/ct2/show... and twice contacted them but no reply.
It really doesn't matter if you detect a met or not - the remedy is the same. If you can't tolerate ADT, you can perhaps get chemo without ADT, but I doubt that it is as effective. Can the side effects you suffer from ADT be managed?
Intolerable ADT SEs were not able to be managed. Tried everything, which is why I stopped and have felt so much healthier without it and remained free of any identifiable metastasis.
Going forward, I'm confident that the 4-drug Care Oncology protocol is a multi-pronged approach to make the PCa a chronic manageable condition. See: careoncology.com/how-it-wor....
Knowing that PSA is an imperfect biomarker, but still the primary metric that oncologists use, what I'm really asking here is this: Does the PSA rise solely indicate cancer activity or, in the absence of any identifiable metastasis, might it be attributable to other factors?
You have had a biochemical recurrence. Whether there is a clinical recurrence has not been determined, but with your adverse initial diagnosis, it has to be strongly suspected. There is an easy way to tell - take some Casodex for just a month. If your PSA goes down while on Casodex, you can be pretty sure that there are micrometastases. Good luck with the cocktail.
Thanks TA. My CO doc had suggested Casodex back in August, which my MO prescribed, but my insurer wouldn't approve since it wasn't 'standard of care' for use by itself. However, I will share your post with her and ask her to resubmit for insurance approval. While I assume that she will understand why you're suggesting this Casodex 'trial', can you pls share with me in just a few words why or how a PSA decrease while on Casodex will indicate presence of micrometastases?
Generic Casodex (bicalutamide) is dirt cheap. It is annoying when insurers refuse to cover something that will save them money, as bicalutamide is surely less costly than SOC. But I doubt you can appeal on that basis alone.
The fact is, even though the FDA only ever approved bical as a 50mg addition to ADT, there are dozens of countries that DID approve it as 150mg monotherapy, and docs in the US have (and still do) sometimes prescribe it this way, off-label, even as its use has fallen in favor of newer, pricier drugs.
My insurer (Cigna) covers mine, as 150mg monotherapy. I pay $7/mo out of pocket for it. Not sure what it would cost without insurance, but perhaps there are other ways to get a discounted price.
If you make an appeal, be sure to include references to papers such as these:
If your PSA increase is due to a benign cause (prostatitis), then Casodex will have no effect on your PSA. It will only reduce your PSA is the PSA increase is from prostate cancer.
Thanks Nalakrats. Based on my own prior experience and some posts on this site, I requested that my MO put me on Cabergoline (prolactin blocker), which I was on a number of years ago and which dramatically lowered my prolactin. Since restarting Cabergoline my prolactin went from 7.1 (Aug) to 0.1 (Oct).
According to the latest AUA guidelines, it appears that for the group of patients in which I fall - Biochemical Recurrence without Metastatic Disease after Exhaustion of Local Treatment Options - items 4 through 8 are applicable, specifically:
Item 7: "For patients with a rising PSA after failure of local therapy and no demonstrated metastatic disease by conventional imaging, clinicians should offer observation or clinical trial enrollment."
Item 8: "ADT should not be routinely initiated in this population (Expert Opinion). However, if ADT is initiated in the absence of metastatic disease, intermittent ADT may be offered in lieu of continuous ADT."
So clinical observation, perhaps combined with a brief trial of Casodex to further identify if micrometastasis is present, seems the prudent path to follow at this time. Thanks all!
Also intolerant of ADT I went on Casodex (combined with dutasteride which is helpful in this setting). It provided nearly 5 years of control before failing and with very minimal SEs.
In addition to PSA testing, recommend CTC testing on a regular basis. Imaging with Ga-PSMA Pet/CT would be helpful and it's now FDA approved at UCSF or UCLA. Best of luck with your case!
I've tried multiple times to get a response from the contact person at this Stanford PSMA clinical trial, but no luck. clinicaltrials.gov/ct2/show... Do you have specific contact info for the PSMA scan at UCSF or UCLA ?
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