PSMA Clinical trial eligibility requires psa to rise to 2.0 above nadir at Stanford/UCLA. Have had nodal Mets previously treated with radiation , adt, and surgically removed. Psa has risen from 0.135 to 0.320 last 3 month's, not on adt. Previous nadir 0.5.
Have 2 options : 1. Adt soon for a period of time, or 2. allow psa to rise to 2.5, psma scan, then adt and possible focal radiation on hot spot(s) .
Doc not excited about letting psa rise this high because of possible spread.
Would like to hear others thoughts please.
Thanks!
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wilcoxsaw
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Really bad idea to wait. You know that systemic treatment with chemo or advanced hormonals will add to your life expectancy and long-term quality of life. There is no evidence that playing whack-a-mole accomplishes anything other than temporarily reducing PSA.
I agree there is certainly a risk, but not sure that some systemic treatment adds to QOL depending on the treatment, in my opinion anyway. Chemo adds about a year to OS and from a prior post here no one responded that they achieved a durable remission after chemo, most respondents gained less than 12 months before a rise in psa began. 5 months of chemo, several months of recovery, to gain a year doesn't make sense to me personally. For others it's a good choice.
Abi spiked my liver, it's off the table. Enza , daro, api are possibilities.
After focal protons to 2 nodes, and 17 months of adt, my psa has taken 38 months to get to 0.320. I still have a prostate, so until my psa exceeds my 0.5 nadir it's unknown if this is from remaining healthy prostate tissue or not. Unfortunately, the psma has a higher psa requirement that my previous C-11 acetate did, hence my inquiry here because of "leaving the barn door open " too long.
I see Dr Dorff on Monday, will see her and Scholz in August. Will see what both say, in the meantime I appreciate all the input.
If the psma did identify a hot spot, it's very likely Rossi at California Proton could treat it, and the psma info would change my treatment direction. Whack a mole has been effective for me so far, to avoid systemic treatment and the decreased QOL each brings with it.
When I wrote that systemic treatment increases QOL, I was not stating my opinion, I was merely repeating what was found by researchers:
"Studies of treatments for mCSPC suggest that the improvements in survival associated with more intensive systemic treatment are accompanied by improvements in QOL. "
Taking polls on a patient forum is not the way to learn anything- those that have had remissions may not continue to participate. Researchers use large random samples. In STAMPEDE, based on 2,962 men with metastatic hormone-sensitive PC, those that had docetaxel+ADT lived 24% longer than those who were only given ADT.
You are making a common mistake in thinking that PSA is cancer (Researchers who should know better make this mistake too). It is easy to "treat PSA" instead of treating your cancer. The larger, visible metastases put out the lion's share of PSA. By ablating those larger, more visible tumors, you will lower your PSA, but are you adding anything to your life expectancy? By delaying systemic therapy, we know for a fact that you are lowering your life expectancy.
Youu wrote: "Unfortunately, the psma has a higher psa requirement that my previous C-11 acetate did," You got that backwards. PSMA can detect macroscopic cancer at much lower PSA than C-11 PET scans (there are no scans that can detect tumors under 4 mm in size):
Thank you tall Allen, you're a wealth of knowledge.
Regarding my C-11 statement, I should have been more clear. What I meant was, the C-11 trial at Phoenix Molecular required psa be 1.0 for me to be eligible for that trial which I did twice. Psma requires my psa to be 2.0 above nadir at Stanford, higher than C-11 did to be eligible.. Hence my concern about "leaving the barn door open" too long in order for the PSMA to be an option. I agree 100%, PSMA is much more sensitive.
Thanks for mentioning the stampede trial, have discussed it at length with oncologist. She has presented at numerous ASCO and other conferences and she said she did not recommend chemo, yet.
She is a big proponent of abi but I can't tolerate it unfortunately.
Fortunately, you can also choose Xtandi or Erleada. An anti-androgen may be less hepatotoxic because they don't directly affect cytochrome enzymes. I really like Tanya Dorff, btw.
Absolutely, and that's in her future plan for me if needed. She's presented on up front intensification but for her reasons doesn't recommend it now in my case.
Yes, Tanya is great, I'm blessed to have her leading my team. Not sure she'll like a 2.1 psa in order to psma, will see her face to face Monday.
Btw, I've followed your posts for quite a while, you're extremely knowledgeable, unbiased, non confrontational, and have helped many. Well done and thank you !
This is what I am struggling with. I can’t make up my mind and am very worried about more waiting to find/zap. The only thing that makes me a bit leaning towards waiting is hearing dr. Myers years ago suggesting that if the DT is more than 12 months then other means than ADT should be looked at.
As usual TA is right. Why wait? But more importantly your premise is wrong. I did a psma scan at ucla less than a year ago at .02 psa. I knew they’d be unlikely to find anything at that low a psa but I weasels starting an ADT vacation and I wanted a baseline to compare for future psma tests. If yuh can pay the $2800 and get a prescription from your dr, you can get a test. They find many mets on men with less than a 2.0 psa
The psma at UCLA is likely not as sensitive as those was using the second generation pyl tracer. Also at a PSA well below 2.0 neither would provide the sensitivity to justify changing treatment for. I'd pay the 2800 but UCLAs might not be my best choice.
I had a PSMA scan last summer at UCLA. I believe my PSA was .7 at the time. They found several mets that were previously not detected. It hasn’t changed my current course of treatment. It sucks finding out this info but now I am aware.
If you only plan to treat with ADT you do not need a PSMA scan. Just have ADT until you are non-metastatic castration resistant.
"2. allow psa to rise to 2.5, psma scan, then adt and possible focal radiation on hot spot(s) ."
If you do that, I expect ADT will work for a longer period because there are fewer tumor cells which can mutate to become castration resistant. You already have invisible micromets in your body and ADT will just stop these to grow to a visible size. I feel it does not make a difference if these grow to a size of 3 to 5 mm so that a PSMA PET/CT can detect them.
I chose the whack-a-mole approach. I did not need Lupron for four years now because the PSA value was reduced by removing the mets instead. Also you feel much better if you know you have no more visible mets plus no side effects from ADT.
Your approach mirrors mine. I plan to use the psma, which incidentally the one at Stanford which uses a second-generation smaller molecule traser seems to be much more sensitive than what UCLA offers, to identify and treat with focal protons. ADT would be added for 12 to 18 months.
Dr Scholz concurs that this PSMA has identified Mets that the older psma has not.
But, the risk is, the barn door is open for a while.
The barn door has been open about two years before the diagnosis of prostate cancer. So I do not think several months until you get to 2.0 will make a difference. I think there is no need to wait for 2.5, you see most of the mets at 2.0 already. See figure 2 in this study:
The reason I'd wait till 2.0 plus nadir is Stanford won't do it until then. And at last look UCLA required the same, perhaps that's changed. Covid has put the trial on hold for a while anyway.
Yes, I trust Dr Dorff. She is a leader in the field, and heads up the trials at City of Hope for CAR T and is head of their dept. Very brilliant lady.
True, but Rossi at California Proton has the expertise and technology to treat a hot spot safely in most cases. He has for me and it has bought me over 3 years with minimal ADT. Certainly not a textbook approach, but an aggressive one.
I too see dr Scholz and I’ve sent numerous people to him whom I follow. It’s not fair to the other readers To imply he advocates a philosophy to “identify and treat” Mets while skipping other systemic treatments as the best way to go. I assure you he does not. He had me use SBRT on my three mets but also had me take chemo , lupron and zytega. He believes the combo can get me to a long term remission and I’m currently on a drug vacation. My point is This may be the best way to go for you and that’s your choice. However it’s not one any mainstream MO would advocate and to imply that it is, could lead someone else here to make that same decision based upon erroneous information. I hope it works for you.
My apologies. I modified my response to not mislead. I did not say " while skipping other treatments" but do not want others to infer that was my intent.
Yes, he also pushes systemic and other treatments.
Schwan, how much peripheral neuropathy did you experience from the taxo, and other side effects.
As I mentioned earlier, Zytiga is not an option for me, and I tend to have adverse reactions to most drugs which is my concern. Lupron caused me cardiac arrhythmias at 17 months. I was one of 3 patients my onc doc saw my liver react to Zytiga out of hundreds she's given it to.
I had only four sessions by design as it was an adjunct to my lupron zytega regimen. No neuropathy and overall It wasn’t horrible. Only two days in bed the whole time. The rest I was able to function pretty well. Usually days 3-4 were the worst. I tried to exercise thru it and mostly succeeded. I even did the cold cap to avoid hair loss and it worked. I iced my fingers and chewed ice during and lots and lots of water before and after.
Right now the Mets are very very small and in problematic areas. Not sure it’s worth the risk at this point. I am going to attempt to have a follow up PSMA scans to keep an eye on what’s going on. Thanks for the advice
I don't know if there is a way onto this European trial, but this contrast agent seems to offer advantage to your situation. Apparently it can pick up lymph mets at 1.5mm. Maybe your onc can get some for a trial?
The PsMa Ga68 PET+CT scan works best where Psa is > 2.0, which is not a high figure considering highest could be 10,000.
Systemic treatment is better than treating each met as it appears in any scan. If there's only a few mets to be seen in a scan, there are often many more that are too small to see, so hammering just 2 with IMRT won't do anything for the rest of the mets. Over time, your body would suffer too much damage with IMRT or EBRT.
The PsMa scan gives a good indication to see if Lu177 will work, and I was told best indication if most of your many mets will be zapped by Lu177 is if Psa < 2 before getting Lu177. In other words, its no use worrying about a low but rising Psa of 2. Most men would have ZERO symptoms of Pca if Psa was up to 20. I've had most of my six PsMa scans so far where Psa was between 5 and 25. Lu177 reduced Psa from 25 to 1.6 last year at 3 months after 4th infusion, and doc said there was not much use in having a 5th shot of Lu177, but said when Psa rises again, and it would do in future,then have more Lu177.
That was last August, Psa went lower to 0.32 in November 2019, while also on Xtandi after 3rd Lu177 infusion, but maybe that's stopped working and so Psa is about 5, rising, so its nearly time to bash the new mets or the old ones that were not killed last time with more Lu177. Research at PeterMac Hospital in Melbourne say this is a valid approach, and said that Lu177 could be repeated twice. If I was to gain mean time of extra 14months of Pca suppression by killing most of it each time, it means keeping Psa low for 42 months, or 3.5years.
Its a better result than I might hope for with chemo.
It I waited until Psa was 25 as it was before I began Lu177 in November 2019, it could 2 years between the time Psa increased to same level as it was before I began, say November 2020, but this might be taking a risk. I can't know if I'd be able to repeat Lu177 2 more times and get 6 more years. I'd be 78. Maybe better to settle for getting more Lu177 in about 2 months, when Psa will be about 10, maybe, it present rate of Psa rise in an indication.
If Xtandi is failing, the rate of Psa increase may slow when Xtandi effect is completely gone, thus leaving the Pca at a slower rate, but the opposite could be said, and if Xtandi is failing, then Psa could rise faster. I just don't know, and docs have told me nothing about this.
But PsMa scans next month will tell me and docs just what is best. It all gets back to scans, and trying to keep Psa low, while watching out for mutant cells that don't make Psa or PsMa. The docs cannot really do any more for you.
I've survived since 2009, Gleason 9, inoperable, Psa 6, Age 62, had ADT, Cosadex, Zytiga, EBRT, salvation IMRT.
From what I saw with my Psa level and PsMa scan results, I doubt the EBRT or IMRT did much except leave me with bowels that are radiation affected.
I had 5 shots of chemo before getting Lu177. Chemo failed, and has caused the worst lasting side effects of dulled leg function.
So, diagnosed in Jan 14 at the age of 57, surgery in Mar 14, T2CNoMx, GS 8, ECE, SV and margins negative, 10% prostate involvement. Surgeon says great pathology report, I won't have any problems....me, I don't like that Mx!
18 months later, PSA comes in at .2, then 90 days later .3. We start SRT in Mar 16, that is an epic failure when 90 days after 39 IMRT and 70.2 Gya, PSA is .7 then 30 days later 1.0...
With PSADT and PSAV climbing fast a trip to Mayo in Jan 17 for C11 Choline scan shows four PLNs but no bone or organ involvement.I had discussed with my medical team here in Kansas City about using a combined therapy of ADT, docataxel and radiation based on the CHAARTED and STAMPEDE studies, their answer, you don't fit the profile so ADT is the SOC.I said I may not fit it now but given my clinical history, GS8, 18 months to BCR, PSADT and PSAV I will be there soon.
Mayo, Dr. Kwon put me on 24 months of ADT, six cycles of taxotere and 25 more radiation treatments (45 GYa, IMRT) which I started immediately. My medical team here in Kansas City was willing to execute the treatment and I would go back to Mayo for subsequent C11 Choline scans and consults.With the first 3 month ADT and taxotere PSA dropped from 4.8 to .8, with the 2nd one, <.1, T to <7. Both stayed there. Dr. Kwon discussed adding Zytiga but based on my response, decided not to. We stopped Lupron at 18 months vice 24 given my response and emerging studies.
Last Lupron was May 18, by Oct 18 T was at 135, by Feb `9 it was 482. PSA has remained undetectable, last test in Jan 20 was .07. Next labs are 4 May.This path was best for me, I chose it, it was aggressive but so was my PCA, not the SOC using NCCN guidelines at the time. I had gone for the cure twice, surgery and SRT, both failed. Is this a cure, who know but certainly it has moved the MPFS down the road, who knows about OS but I believe it has moved that too since given my clinical data I believe I was headed for an outcome that would not be good.
Yes, the chemotherapy and docataxel had their SEs but other than travel restrictions during radiation treatment, I continued to work, travel, exercise, vacation.
I feel like I am in AS now, my urologist and I test and consult every four months, labs on 5 May had PSA at .07. We have an idea of what we'll do when it comes back, get multiple readings to gauge PSADT and PSAV, image using C11 Choline, Aximun or PMSA, then informed by that clinical data, make a decision on treatment.
The C11 Choline scan enabled my radiologist to build a better treatment plan with wider margins and boosts to the four PLNs, we treated all PLNs, not just the four. The ADT and docataxel were based on systemic PCa, no doubt it was elsewhere as micro metastatic PCa, too small for the C11 Choline scan to pick up.
By ending ADT I may be playing whack a mole but I can't begin to describe how good I've felt since the Lupron cleared my system. For me, the combined regimen and systemic treatment vice monotherapy of radiation to the PLNs wa the right choice,
Not sure, one would think that with the rise to 482 my PSA would return to its old ways with rapid doubling and velocity times.
With the February results I was mentally resigned to in the near future having to image and then decide on treatments.
The subsequent decline and stabilization has baffled me though I am happy. I asked my urologist if he had any ideas, no, just continue doing what you’re doing!
I do eat reasonably healthy and I exercise frequently but don’t think that is the reason. Perhaps the combined regimen of taxotere, Lupron and radiation reduced my PCa to a point where my immune system can keep it under control.
I agree with Tall .... if PSA roughly corresponds to tumor load, waiting from a PSA of 0.32 to a PSA of 2.0 would be waiting for the tumor to get over 6x bigger (over 500% growth).
I had a PSMA PET CT scan at UCSF in January. They had no requirements on PSA level; I only needed a doctor's referral which included evidence of prior PCa. My PSA was around 0.6 at the time. UCSF (China basin) isn't far from Stanford.
Yes. Her name is Raven Smith, phone 415-353-9448. Sometimes she is difficult to reach, so an alternative is Siddiqua Khadija, phone 415-476-4302. The latter was a bit difficult for me to understand because of her accent, but she also is very friendly and helpful.
BTW, the cost at UCSF is $800-900 (assuming you have Medicare) and that is substantially less than UCLA. As it turned out, my insurance (including Medicare) paid ALL the charges.
I was worried because of a 30 day doubling time, but it turned out that I had only a single spot, on the 3rd left rib. Had that radiated in February and after only 2 months my PSA fell to 0.034. The radiation oncologist said to wait at least 2 months to see a decline and the full decline will take longer. I suspect i will be undetectable on the next measurement.
I was on intermittent ADT after radiation and psa increased rapidly due to bone mets . Being tired of ADT side effects and knowing that I needed lifetime ADT I switched to estradiol patches so I can stay on them until they no longer work with very few of the side effects of Lupron and it’s ilk. I waited til psa was high enough for PSMA or axumin scans or even mri to be effective in finding mets. It does help find treatable mets but you need systemic treatment to treat microscopic mets which can’t be seen but are there in the millions.
If you haven't progressed on ADT it's probably time to re-start that immediately. You may get much more time until you become castrate resistant. After that there are plenty of tools in the toolbox for your systemic disease, such as chemo and the second-line hormonals Tall_Allen mentions.
Have the PSMA PET scan now. I had my first scan against advice to wait until PSA rose to 2 ng/ml, because accuracy of the test was poor at lower levels (eg sensitivity and specificity 50% at my PSA level of 0.3 at the time. I had 7 soft tissue pelvic PC lesions. Early is bes,t and it allowed me to have Lu177 treatment where PSMA avidity is required for success. Seems as though you have plenty of comment which I don't have time to read
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PSMA PET CT versus PSMA PET MRI
PSMA PET SCAN AND PSA
PSMA PET-CT Ga68 Scan results
If ADT can \"hide\" mets on PSMA PET CT, lesions can still be seen on MRI, no?
Rising PSA … Clear PSMA SCAN
