uPSA Rising : Treat now or Wait for T... - Advanced Prostate...

Advanced Prostate Cancer

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uPSA Rising : Treat now or Wait for Tumor to Grow

RMontana profile image

I have had a RP, recurring PSA of 0.13, ADT for 6 months, had a clear PSMA PET (Jan 21), then RT IMRT for 34 days with a total of 68 PSA is now starting at ultra low levels, but is slowly rising...I read that IF it gets back to 0.03-0.05 ng/ml THEN I will most likely have BCR...meaning the cancer is still Oncologist says to just wait, let the PSA rise to 0.15-0.20, then go back and get a PSMA PET...OK, but...

...if I get to 0.03-0.05 what should I do...just wait and let it rise and form a tumor I can find with a PSMA PET? Or do I go back on ADT (which I tolerated well for 6 months) and keep PSA low? Has anyone out there gone thru this phase and what happened to you; what would you have done differently? TNX

42 Replies

Your PSA isn't worth doing anything about.

RMontana profile image
RMontana in reply to Tall_Allen

...what else do we have...tell me please...

Thinus profile image
Thinus in reply to Tall_Allen


I had salvage after my radical, but my RO uses an assay that records ONLY is it is .09 or below.

RMontana profile image
RMontana in reply to spinosa

...correct, but I am in Panama and here they give you PSA down to the thousands of ng' mine restarted at 0.003 and is now pushing .01, so here we go again...I read that if it gets back to 0.03 (USA) and 0.05 (Japan) research shows likely hood of BCR...that means the cancer is still out there...somewhere...then my choice is once again (like the good old days monitoring my rising PSA) to just wait, let a tumor grow and try to find it...dont know what to do...just asking if going back on ADT to stop PSA rise should be considered...then again, is ADT palliative or a cure? Any ideas...

maley2711 profile image
maley2711 in reply to RMontana

ADT is not a cure....but a blockade that may hold for a variable number of months/years.

cancerpreventionresearch.aa.... I take this.

Very good article; I took away these items of interest...

The , primary endpoint was not reached most likely due to;- unexpected PSA variability at M1,

- to a relatively short intervention time (6 months) and

- small number of patients involved in the trial.

- Primary Endpoint was PSA Slope change; study reached −0.0162 log, rather than the expected -0.012 log (ng/mL)/month [still darn close]


- The difference in the log PSA slopes became significant when PSA values measured at M1 were omitted (M0–M3–M6 or M0–M6) from the calculation.

- The resulting PSA doubling time increase was substantial (almost double).

- With M1 excluded; the PSA doubling times were 31.9 and 16.6 months in sulforaphane and placebo groups, respectively (+92% increase).

- A stabilized free-form sulphoraphane is a valuable asset in anticancer prevention and therapy.

Natural Products...this was also in the study which really gets me interested...

- Only sulforaphane precursors such as purified glucosinolates or broccoli sprouts and not sulforaphane are currently in intervention trials.

- The bioavailability of sulforaphane is therefore dependent on the presence of myrosinase or gut thioglucosidases, which convert glucosinolate to sulforaphane.

- In this setting, measurement of urinary levels of dithiocarbamates (sulforaphane metabolites) indicated striking interindividual differences in bioavailability.

- Cruciferous vegetables contain glucosinolates which was originally isolated from broccoli and is produced from glucoraphanin, its glucosinolate precursor...

- Glucoraphanin is converted to sulforaphane by myrosinase, but myrosinase is denatured by cooking, and when intact glucoraphanin is ingested, it is eventually converted to sulforaphane by gut microbial thioglucosidases.

- Myrosinase is a family of enzymes involved in plant defense against herbivores...

- In a double-blind placebo-controlled study, green tea catechins (GTC) significantly prevented prostate cancer development in men with high-grade premalignant prostate intraepithelial neoplasia (PIN 42).

Take Away;

- eat raw broccoli; lots of it.

- drink high quality green tea; look for the GTC content.

- doubling time for PSA was very pronounced, even if the primary end point was not reached (it was sort of arbitrary to begin with).

- only a "stabilized free-form" sulphoraphane will idea what this means, but patients are given this as a medication it must meet this requirement.

- barring getting this as a medication follow the natural products pathway...there is a larger follow on study in the works; this one was done in France.

Thanks for that detailed take. Not that I understand it all. In my simple mind, I see a RCT with real people (yes not huge number but enough to draw some conclusions) with my very issues also, and they take 60mg of a product that is now available in the US on Amazon from the French manufacturer of the actual product used in this study (BROQ-not inexpensive stuff at 3 bottles/mo), and have what I consider good results compared to control group (doing nothing). Why not just duplicate what they did, but dont stop at 6 months? No measuring, worrying about conversion, bioavailability, etc. I love broccoli and eat that also, but to get the mg dosage that showed results in this study, I think I would have to back up a truck load full and my wife would end that quickly. Until the new study you reference comes out with good results, and is doable, I guess no harm in following this protocol. Thanks for the tip on GTC. I will have to look at the study to see what content gets the result.

Wow...I see BROQ on Amazon...the surgeon who operated on me had 3 papers published; ALL were on the effects of green tea on prostate cancer, which is why I zeroed in on that one...but, am interested in your product for sure...TNX

It almost seems too simple which is why I look for other input. I have heard generally about green tea being good for all but not prostate cancer in particular. Can you share surgeon name so I can look up the studies? If not, I am sure I can find info. Thanks.

RMontana profile image
RMontana in reply to RMontana

By the way, forgot to ask, how is it working for you? You state 'good results,' but if I can ask how good? The study had its best results in slowing the doubling time...have you seen this in your case; you dont have to be specific. But, has your PSA slowed down, or at least stopped going up as fast...or has the PSA been kept down to levels that make you think its working...just want to know as I am going to buy this stuff...

As for putting Dr's names on here...that's something I dont want to do now...I vent a lot and they may not think it fair and I really have to take my complaints to them personally, so I would rather not state the name...but there is more than a bit of information written on this for sure...he was not the first one I saw with a connection between green tea and prostate cancer cells...TNX

My PSA is now 18 & I do not think you have anything to worry about but I shared your concern when a scan showed a spot on my left collar bone that had come from prostate cancer.My understanding of ADT is it lowers the PSA numbers but does not kill a tumour. It all just buys us time on this planet

Had I have had a third shot of LU177 I believe my PSA would not be 18. Would it have killed the tumour? Good question...

RMontana profile image
RMontana in reply to ARIES29

...I have been following LU177 for a while; I actually had a PSMA PET scan at UCLA, which uses the same protein, but with GA168 attached...the difference is at annihilation the GA168 puts off light (so you can find the tumor) and LU177 puts out that what you understand? But where were you treated and you were treated twice! Tell me more...TNX

marnieg46 profile image
marnieg46 in reply to RMontana

You might find this video interesting if you haven't seen it already...

RMontana profile image
RMontana in reply to marnieg46

...very interesting...I took away this;

"Phase III VISION study with 177Lu-PSMA-617 met both primary endpoints, significantly improving overall survival (OS) and radiographic progression-free survival (rPFS) in patients with PSMA-positive metastatic castration-resistant prostate cancer."

So they did phase III trials! But back to had two sessions and you think a 3d would have reduced it more...why did you not proceed with a 3d and where did you get treated for the 1st and 2d. TNX

marnieg46 profile image
marnieg46 in reply to RMontana

Bit of a misunderstanding... but my husband hasn't had Lu 177 but rather has had 3 PSMA scans...first in 2015. Since 2019 his only treatment has been Lucrin (lupron). We're in Sydney and lutetium treatment is available without too much difficulty, although costly, and it will probably be something that he has to consider in the future.

You did pick up what many miss...while some dismiss the benefits of the basic outcome in the VISION trial or comment on just the OS of a few months it needs to be remembered that this came for men who have been heavily treated and with very limited options but it's the secondary outcomes that were so promising..especially the rPFS and promise of future developments in this area. I think one will be definitely moving Lu177 much earlier in the treatment paradigm.

There is an excellent video from UroToday by Michael Morris that really brought home for me moving beyond just using OS as the benchmark of whether a treatment is worthwhile…

Trust all goes well for you on this journey and the choices you make are just right for you.

RMontana profile image
RMontana in reply to marnieg46

TNX! Great pull lines;

1. The hazard ratio was 0.62, which in plain terms meant that the risk of dying was reduced by 40% in favor of receiving the combination of the standard of care, plus lutetium PSMA. 2. For radiographic progression-free survival, which is the time from randomization to either radiographic progression or death, the hazard ratio was 0.4. So a 60% improvement in the likelihood of remaining free of radiographic progression or death.

3. Control Arm; over 50% of the patients who were assigned to the standard of care alone arm, dropped out. Needed re-education of the investigators; that patient would still get really good medical oncology care and would be able to participate in this study. That dropout rate went from 56% to 16%.

That last one is know the patients were talking to each other and so the only way they got the 'Control Group' to stay was to offer them the treatment being many times does that happen...

Lastly, how sad that right now we are limited to using this treatment for 'end of life; conditions, when all else has failed...but at the end of the presentation was this gem...Cheers

Dr Morris; "This trial was in patients who had really very few viable treatment options remaining to them. And this shows that this new drug class for prostate cancer, radio-targeted, radioligand therapy, opens up a real doorway, not only for these patients who have completed an androgen receptor pathway inhibitor, plus chemotherapy, but it opens up the doorway also to future studies, looking at this therapy earlier in the disease. And we've generally found that when we move a drug from this late population to an earlier population, that those clinical benefits can be amplified..."

marnieg46 profile image
marnieg46 in reply to RMontana

An interesting and very informative review.. you should keep a look out for others posting and asking questions about Lu 177 and the VISION outcomes and raising doubts it is of much benefit by just focussing on the OS...they'd benefit from and be encouraged by your analysis. Secondary endpoints were pretty amazing especially given the cohort.

Yes. A clever tactic to keep the control group involved. I'd missed that point. Probably doesn't happen much but a real incentive for them to stay the course.

Trials are presently taking place at the Peter Mac Centre in Melbourne involving using Lu 177 for men who are at earlier stages and still hormone sensitive. I've read that there is also some thought it might be effective prior to what a game changer that could be. I guess it's only through the success of trials that this treatment will be an option for many and hopefully when that does happen it's affordable.

One day this affliction, will surely become for many more men, a chronic rather than a terminal condition. Let's hope that day comes sooner rather than later until there's a proven cure.

ARIES29 profile image
ARIES29 in reply to RMontana

My second treatment of LU177 was in 2016 & PSA was down to 1.6 from 19 before the first treatment. Why they did not continue is a mystery to me but I have a page of explanations from a Dr Macfarlane, nuclear medicine physician from Theranostics here in Australia.Personally I believe it was a clash of personalities? The oath of Duty Of Care to a patient did not apply to me.

I was told that although lutetium-177 PSMA could produce long term-remission it is a palliativa agent & therefore cyclic androgen deprivation might be feasible or chemotherapy.

Now I am taking fermagon shots monthly & that was my reward for daring to think outside the box & find a treatment that works.

Thankyou LU177 for giving me those extra years & I sincerely hope Dr Macfarlane MBBS from GenisisCare, Theranostics, Australia suffers from the same disease only to be told he can not have it.

RMontana profile image
RMontana in reply to ARIES29 only blessing I have in the USA is that I can just bloody well go pay for the treatment if I want...dont know how costly that is, but we pay for a lot of things that are equally costly and dont extend your life...I empathize with you...I am way behind you in line and need to learn from what you have gone thru...thanks for sharing helps me stand to my OC who just wants me to sit and wait and let the PSA grow and then deal with it...I differ with that approach and will seek treatment where I think it best serves me...there are no treatments that are free from side effects, but mortality is the ultimate complication...Cheers

ARIES29 profile image
ARIES29 in reply to RMontana

With a start out PSA of 19 & two treatments of LU-177 reducing it to 1.6 why would it not have reduced it further?? I will never know & for my reduced years of life I can thank Dr David MacfarlaneMBBS of Theranostics, Australia.Would not anybody be pissed off in this situation?

Here's a good paper to read on detection limits of PSMA imaging.

At present, PSA levels ≤0.2 ng/ml are frequently judged in postoperative patients to be non-critical, nevertheless one-third of our patients (33.3%) had PET-positive findings even below a PSA of 0.2 ng/ml. This rate drastically increased up to 69.2% in patients with a PSA level between 0.51–1.0 ng/ml. Thus, PSMA PET/CT detects early local recurrence or metastatic disease and possibly allows for a more effective and early treatment.

My MO recommends a PSMA scan at PSA = 0.7.

Cooolone profile image
Cooolone in reply to timotur

Nice Retrospective Study...

But I disagree in part, see quote:

"Since all data available consistently document that PSA control is significantly better when radiotherapy is commenced as early as possible, it is not justified to wait until PSA is in an optimal diagnostic range. Our strategy to cope with this dilemma is therefore to employ PSMA PET/CT in patients even around 0.2 ng/ml especially whenever high-risk features are present."

When the data shows a +2x detection rate at the threshold of .5 vs .2ng...

The study advocates getting the PSMA scan as low as .2ng, but by doing so a patient may miss a big part of the picture of what is causing the PSA increase. Additionally, the study does not identify lesion detection sizes at what sensitivity levels, something also useful but not necessary for making decisions.

It's advocacy for using the scan at a 33% detection level is irresponsible IMO, and I'm not sure how this position could be supported when tracking and waiting for progression to just .5ng (+.2ng) provides such significant better efficacy in results. This small rise in PSA is unlikely to contribute any significant difference in PSA control via salvage therapy again, my opinion.

Interesting study nonetheless, especially for highlighting some statistical information, thanks for posting.

RMontana profile image
RMontana in reply to timotur

Thank! My current Urologist told me that, if get back up to my post operative, recurrent rate of 0.13 ng/ml, he would send me for a PSMA PET at that point...I agree and my background has been consistently helping populate the FAR LEFT sliver of the statistical bell if something is stated to only apply to 3, 4, 5% of men, THAT's ME! Well, someone has to do it, but joking aside, I am fed up with being the, what you sent me is good to know...I a NOT gonna wait for my PSA to go up to .20, or 1.0, or whatever....once it goes up it DOES NOT come back, will keep an eye out...have copied your post...TNX

PS from conclusions; There is an almost linear increase of PET-positive result with rising PSA level: Patients with PSA ≤ 0.2 ng/ml had a detection rate of 33.3%, patients with PSA 0.21 ≤ 0.5 ng/ml a rate of 41.2% and patients with PSA 0.51 ≤ 1.0 ng/ml a rate of 69.2%.

Sooo, it looks like I would be risking a NEG result, but there is a 33.3% (1/3d) chance that even at that level it would find something...out of pocket the scan costs $3300...not insignificant, but my cell phone cost me $ will see...TNX2

Thinus profile image
Thinus in reply to timotur

Thank you, informative

.05ng is the threshold considered to be "detectable"... And TA has made you aware that at your current level, being below this, isn't anything to be concerned over.

Take that suggestion with the highest consideration! There will be plenty of time to worry, should you ever need to, but reserve it for then. Right now, breathing and going about doing some of the things you enjoy, and enjoying them without incessant fixation on your condition will help your mind relax! And the mind is a terrible thing to waste...

And your doctor is incorrect about the PSMA scan. At .1-.2ng your PSA will still be too low for any scan to offer any insight or see anything. The best scan, G68-PSMA-PET threshold begins at .5ng and is better at .8ng than others (noted above). So even if your PSA continues to climb, you have time to wait, yes wait, in order to be able to SEE what's causing your PSA to rise.

Good luck!

RMontana profile image
RMontana in reply to Cooolone trying to relax as you say, but have been an outlier at every single step of this disease...has got me flummoxed...but, you are right; its 70% Specificity at 0.5 PSA and 87% at higher is 'better...' in a way...TNX

My mo only looks at psa down to <0.1 …. He says they aren’t interested in psa’s below that and those should be ignored. The ten or so guys I know with PCa do it the same way. My Mo says if it starts doing 0.2 , 0.4 , 0.8 etc. then he would think about changes when it hit 2.0 . I’ve been at <0.1 now for 32 months straight , while on debilitating adt.

RMontana profile image
RMontana in reply to Kaliber

...OK...I had ADT for only 6 months and tolerated it OK...some hot flashes and I grew breasts! Little ones, but they are there...I was thinking of going on ADT if it rises and not let the PSA to back up to .50 and 1.0 and up...why wait...but ADT has its impacts as well...its not a cure for tumors, but I still cant get a straight answer if its a cure for PCa cells...before they aggregate into tumors...dont know...TNX

Kaliber profile image
Kaliber in reply to RMontana

At this point in time , if you have advanced stage 4 metastatic prostrate cancer … there is no cure at all. No one walks away from APCa .

There are many schools of thought on adt , ….vacations, intermittent etc. my personal view is if you go on adt and it works ….stay on it until it quits. Every time you stop you are inviting the cancer to start growing again , often very rapidly after adt. If you have your shoe on its neck and have it down ,,, keep it there as long as you can. It’ll eventually find a way around your adt , but adt is all about helping you have a little longer life. I’d exploit that to the max. Just IMHO.

RMontana profile image
RMontana in reply to Kaliber

...exactly...I dont have APCa and that is my driving goal in what remains of my life, NOT to advance to that stage...I am now asked to just wait and let the PSA rise, then 'deal with it...' Why? Plenty of studies show that if ultra low PSA after RP surgery and RT radiation, rises to 0.03 in the USA (and 0.05 in Japan) that you are on your way to, why not just start ADT and keep the PSA low...

There is also a blood test for free floating PCa cells....very hard to get and I think its only available in one Tennessee Lab (cant recall now the name)...THAT would interest I have these things floating around? If I am on ADT can I get tested every 6 months, every year and determine if its killing the cells...OR keeping them low...dont know, but I cant get anyone who treats me interested...not in the them just sit and wait...yeah, right...

I saved your text...that is my philosophy...dont wait and fight this enemy before its reinforcements from what I read there are now 3-4 other hormone treatment regimes that can be used as PCa finds its way around some...try TNX...

PS are you now on ADT? How long have you been on it? Which drug did you take? What was your experience? TNX2

Kaliber profile image
Kaliber in reply to RMontana

Ah …. that explains a lot. Of course everyone is very welcome here and always encouraged to join if you are so inclined. We always want everyone to feel comfortable here. This group is mainly populated by people with “ advanced “ PCa and are living out their final moments before death. All of us realize we are croakers sharing the companionship of others facing certain , and possibly impending, death as well. Seems like every week there is sad news of another loved brother warrior passing. It’d be difficult for me to comment much on your circumstances since mine are so dramatically different.

I’m on Lupron Xtandi Zometa . I was severely cancer damaged when DXed…. being very late in detection. My medical team wanted me to enter hospice immediately. I was very sick and in a great deal of pain too. Having never had an attempt at treatment, I opted for a try at adt. I turned out to be a super responder and my 1600 psa dropped to <0.1 in about 2-3 months. I’ve escaped hospice for 32 months , so far. I’m tested every 30 days.

There is another cancer group here that , like you, aren’t “ advanced “ ( facing death ) but are still serious prostrate cancer, that might have more in common with your circumstances as well.

Keep up the good fight brother warrior 💪💪💪❤️❤️❤️

RMontana profile image
RMontana in reply to Kaliber

...OK, did not know this was an advanced cancer group...there could be advantages for me though in that I can look at the paths you all have trod and see if there is a way for me to take another only claim to panic is my Decipher score, which was a staggering 0.97 out of 1.00; off the charts aggressive cancer compared to my visual Gleason grade which was more 'vanilla' 4-3; my Dr's to this day wont explain to me HOW the two can be sooooooo totally opposite...but, I trust that the genome markers are more accurate and I discarded the Gleason...but I digress...

...I must seem like such a whiner to those out there with advanced disease...I beg your patience and understanding...I do though want to learn as much as I can from your journey and if there is any way I can take action now to avoid a journey on the same route that would be of help...I am not getting any help from my Doctors...not that they dont know what's coming, but that their attitude is that its best for me not to worry...they remind me of the old Greyhound Bus commercials;'...just leave the driving to us.' Well, I cant and have to search out what's out there and if anyone with advanced disease can help me not make a irreversible choice now, that would pay off big later, that's what I am Decipher score hovers over me and casts a constant shadow on any other seemingly 'low risk,' metric I currently display...if I get this wrong, if this thing gets away from me, I'm toast, so I am darn well not going to sit back, kick my feet up and wait for symptoms to identify additional treatment...not wired that way...

...but, I will try to determine how to even find forums that are at different levels of progression...will learn there too and may be of help as well to others in my same progression class...if anyone has a lead on this, please advise...TNX

Kaliber profile image
Kaliber in reply to RMontana

I know there are other groups here that aren’t stage 4 …. It I forget what they are. Try pm-ing the moderator Darryl and explain you are “ advanced “ and are looking for the most suitable group. I’m sure he will be happy to help.


I’m curious why you stopped your ADT after six months? You said you were tolerating it well. I thought two years on ADT was the SOC? At least that’s the plan by my MO. Best wishes to you!

RMontana profile image
RMontana in reply to bean1008

...that was my question...but my OC oncologist said 'no mas...' so I went from ADT to RT radiation (34 doses of 2 Gy), then cold turkey...his approach is, 'wait of it to rise, get a PSMA PET and go from there...I am not convinced...if I tolerate Lupron well [not many side effects and my small breasts could have been prevented] then why not stay on it longer...even 2-3 years is a LONG time to kick this can down the road...meanwhile science moves forward...I am going to get another OC...will keep pushing...if I dont, who will...TNX

Cooolone profile image
Cooolone in reply to bean1008

The SPPORT RTOG0534 trial showed very good results for patients post RP with recurrence for a short course (6 month) ADT intervention along with RT especially to the lymph nodes. Results so good in controlling further progression, they released the study results early so patients could benefit and pushed for this to be SOC. Of course that was years ago already, but some practices follow this... I don't remember the numbers off hand but they were very compelling.

But this example is weird because it doesn't follow that exactly. In the trial, the ADT is given while RT is applied as well, usually ADT prior to beginning RT and the ADT lasting past the completion of RT... The combined modality being much more effective than mono therapies.

RMontana profile image
RMontana in reply to Cooolone

..with you brother...I asked my OC for more ADT...he said flat out 'the band plays on...' as was the case with another disease...why I am not continuing with ADT is beyond me...but let me see what happens with my least in Panama, where I live and work, they report PSA down to the 10th of my first post RT PSA was 0.003...but my second was 0.009; triple! Waiting for my third...but I feel I am back in the 'good old days,' of watching the on coming train wreck, which was my yearly DRE & PSA scam...dont get me started on that...Cheers

bean1008 profile image
bean1008 in reply to RMontana

RMontana, did they stop the ADT possibly due to blood tests showing bad effects on your kidneys or liver?

RMontana profile image
RMontana in reply to bean1008 OC just flatly refused to consider continuing it...I am to sit and ride the dragon until it either lands and release me to stumble into my 80's, or takes me to the realm of advanced prostate cancer, where I now realize most in this cohort reside...but, that is what galls me...I dont get a say in what action to take during this next phase of my disease...I am so far refusing to accept this protocol...dont know what else to do yet, but I'm working on it...yet, am I being this the 'best' option for me...wish I was more certain; I would not be typing right now if I were...

My PSA is .11 and my oncologist says even a PSMA Galium scan won't detect. Then why the Boe scan and MRI of prostate bed?

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