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CT PET efficiency with PSMA, c11 choline and axumin

Break60 profile image
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I’ve asked this in the context of a response but decided to start a new thread having received only one comment:

Data show that the efficiency of these scans increases as PSA increases but no further improvement is evidenced above I believe the 2.0-4.0 range.

Is there any evidence that waiting for PSA to reach say 2.0 before getting the scan and starting treatment is dangerous and reduces overall survival?

Bob

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Break60 profile image
Break60
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Tall_Allen profile image
Tall_Allen

This article has a chart that shows the relationship between detection rates and the type of scan:

pcnrv.blogspot.com/2016/12/...

The TOAD study examined immediate vs delayed ADT:

thelancet.com/journals/lano...

Break60 profile image
Break60 in reply to Tall_Allen

TA

Thanks for the outstanding analysis.

The TOAD trial if I understand it correctly divided two cohorts equally into (a) those getting immediate ADT and (b) those getting ADT after a delay of two years. Five year overall survival for the two groups was 92.1 % and 86.2 % respectively.

Question:

1. Why in the real world would anyone with progression wait two years to start ADT?

2. I’m surprised the OS difference was so small yet immediate ADT was considered to be significantly better. Is 86 vs 92 significant ?

For me to get a productive ct pet scan by waiting until Psa reached 2.0 I’d only be delaying ADT by six months at most assuming a doubling rate of two months. I don’t consider six months an inordinate delay in light of TOAD.

I’m sure you think that a two month doubling time is very troubling in itself but it hasn’t proved to be so for me. Twice I’ve waited a few months for Psa to rise to a level where mets were detectable radiographically , started ADT3, and radiated the mets. I suppose you could say it’s not clear what killed the oligomets: ADT3 or radiation . I would think that the combo killer them.

Finally, you say sbrt is a reasonable option for those with oligomets which can be treated safely yet you say it’s not proven to be effective. Huh?

Bob

Tall_Allen profile image
Tall_Allen in reply to Break60

You didn't mention mets in your original post. TOAD was in men without metastases (which is why the overall survival was so high in both groups) in just 5 years of f/u. Metastases is considered a reason to start ADT. Looking at OS the other way - mortality rates doubled for those who waited. But it's just 5 years - too soon to draw conclusions.

Waiting for a scan to pick up mets with a 2 month doubling time is not warranted by any evidence. What do you hope to achieve? It is a self-fulfilling prophesy - you will have more detectable mets the longer you wait.

Break60 profile image
Break60 in reply to Tall_Allen

So far my detectable mets by scan have been few: 2 in 2015 and 1 in 2017. That’s why I’m optimistic that I’ll have few again which will be treatable by ADT and radiation.

Tall_Allen profile image
Tall_Allen in reply to Break60

"treatable"? You can zap anything - but that doesn't men you've increased your expected survival.

cesanon profile image
cesanon in reply to Tall_Allen

"You can zap anything - but that doesn't men you've increased your expected survival." Tall_Allen

How can that be? Why would that be?

Break60 profile image
Break60 in reply to Tall_Allen

I don’t believe you’re correct. Some did have mets and some were designated as not curable . It was a cross section if all phases of PCa.

cesanon profile image
cesanon in reply to Tall_Allen

Tall Allen's link:

pcnrv.blogspot.com/2016/12/...

Is the best compilation of information on this subject available on the internet.

Break60 profile image
Break60 in reply to cesanon

Yes that’s TA’s analysis which I agree is very informative. But I question some of his conclusions which I’ve tried to explain above. PCa as we all know is very slow growing. I believe (as do many others ) that these new scans are an important new way to find mets which can be treated with radiation . I’ve not been a fan of delaying systemic treatment however. What’s the point of improving scan accuracy to find mets sooner if you don’t use that info to change or augment treatment modality?

cesanon profile image
cesanon in reply to Break60

"But I question some of his conclusions which I’ve tried to explain above. PCa as we all know is very slow growing. I believe (as do many others ) that these new scans are an important new way to find mets which can be treated with radiation . I’ve not been a fan of delaying systemic treatment however. What’s the point of improving scan accuracy to find mets sooner if you don’t use that info to change or augment treatment modality?" Break60

Break60, may I ask you to restate that using different words. I think you are saying something important, but I am not quite picking it up.

Break60 profile image
Break60 in reply to cesanon

If you look at the many clinical trials currently underway for the new ct pet tracers like Ga 68 PSMA, axumin , etc. , their goal is to see if treatment plans changed as a result of these scans compared to standard bone scans , MRIs etc. . So far , results are promising in that treatment plans have changed in a significant percentage of cases. So as a result of these new tracers (if that’s the correct term) the cancer is now getting discovered earlier , treated earlier and treated more aggressively which should increase survival.

As Psa increases, these new scans are more accurate ( up to Psa of 2-4) but they find cancer at much lower Psa levels than older methodologies: As low as .2. In fact, in order to qualify for these trials your Psa must be at least .2 for two successive tests. But they’re expensive so one would like to get as accurate a scan as possible for their money. Of the newest tracers only axumin is FDA approved and paid by insurance.

My argument with TA is about how long to wait to start therapy with high risk PCa. I’m trying to balance waiting time with diagnostic accuracy. Plus I have more faith in focal radiation of oligomets than he does because it’s unproven. But it’s worked for me.

Bob

Tall_Allen profile image
Tall_Allen in reply to Break60

I can only tell you what we know so far. So far, the only kind of therapy that we know increases survival is SYSTEMIC therapy. The evidence from metastasis-directed therapy (MDT) so far is that the increase in survival, if any, is minimal. Metastases crop up slowly at first anyway, whether one picks them off or not (at 5 years, only 15% of MDT-treated men still had progression-free survival.) There has only been one pilot randomized trial so far to help determine its effectiveness, which you can read about here:

pcnrv.blogspot.com/2017/12/...

It is important that patients understand the very real risk of avoiding systemic treatment when there are known metastases. While it risks little to treat those oligometastases that can be safely treated, we must understand that there is no known survival benefit to doing so. There is a known risk to delaying systemic therapy. Dr. Ost wrote to me, "MDT does not replace ADT and our results should not be interpreted in that way."

Break60 profile image
Break60 in reply to Tall_Allen

I agree. I augment ADT with RT. I don’t replace it with RT.

Break60 profile image
Break60 in reply to Tall_Allen

TA

I had gs 4/5 at pathology but 3/4 at the 4mm margin. Would lower g score at the margin (at the base where there was EPE) have any bearing on the aggressiveness/quantity of mets? Or does the gs of the gland dictate type/ severity of progression? Or is it impossible to know?

Bob

Tall_Allen profile image
Tall_Allen in reply to Break60

The presence of Gleason pattern 4 at the margin means the cancer there can progress to a point where it metastasizes. It's possible that some metastasis -capable cells escaped from elsewhere too.

Break60 profile image
Break60 in reply to Tall_Allen

I was just wondering if the fact that I had no Gs 5 at the margin helped account for the few mets I’ve experienced in spite of having SVI and Gs 4+5 in the dear departed gland. I’ve had no recurrence in the bed or the lymph nodes or new mets in any other soft tissue or organs.

Tall_Allen profile image
Tall_Allen in reply to Break60

Metastatic progression is usually slow at first and speeds up later.

Thinus profile image
Thinus in reply to Tall_Allen

Allow me a word here. When bone mets start showing up on scans, you can be sure that your lymph nodes are affected already. It is the work of the lymph to absorb as many poison as possible. Out of experience I know what happens if you skip one ADT injection. When your testosterone comes back in circulation, the doubling time is 2 every week. Long story short: if there are still visible bone mets, stay on ADT.

Break60 profile image
Break60 in reply to Thinus

When two iliac nodes were imaged by MRI in 2015 I had ALL my pelvic lymph nodes nodes zapped with a total of 75 grays over 50 sessions and went back on ADT3 for 13 months. When I had recurrence again a scan with axumin in 2017 located a single 9mm femur met which was treated with 27 grays of SBRT in three sessions and another thirteen months of ADT3. No other mets were seen anywhere. I fully understand the importance of systemic treatment but I choose to supplement it with radiation if it can be done without harm.

Bob

Thinus profile image
Thinus in reply to Break60

Well it looks as if you are on top of it, which is the most important. You get guys that stuck their head in the ground like an ostrich and think the problem will just go away. I am now on a drug holiday of 90 days, but I am making Dischem rich here in SA with all the herbs and supplements I throw down my throat. On weekends I give my stomach a break and just float through with the capsaicin and lycopene.

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