My Lu -PSMA therapy hasn't been successful at controlling my cancer. During treatment my PSA and ALP continued to rise dramatically. I have an Axumin scan at the end of the month to look at the non - PSMA cancer extent.
I'm now starting cabazitaxel to hold the cancer at bay while I wait to join a trial. I spoke with City of Hope about joining their CAR -T trial, for which it looks like I would be a good candidate. I'm also reaching out to MD Anderson to ask about PT112, and what other trials might be appropriate.
I recall some members on the forum saying they are in the PT112 trial. Id like hear about their experience.
Written by
Javelin18
To view profiles and participate in discussions please or .
So many on this forum are hoping for FDA approval for LU177 so it will soon become widely available, maybe by June. Clearly, and unfortunately, it does not appear to be widely effective. I just finished a trial using Actinium225, a brother of LU177. It didn't work for me.
I am also starting Cabazitaxl, along with Carboplatin, in a few days at CINJ. I have to admit that when I was first told that I needed systemic treatment using chemo, I had no idea if there would be another available/viable treatment after it. But then I reminded myself of all the current and coming trials that are out there. This is an amazing time for us all to reflect on the progress being made for treating prostate cancer. None of us should be afraid to consider and participate in a clinical trial.
As always, I am researching my next treatment options and mulling around my next plan B. CAR-T is on my list. Of course, my upcoming chemo treatments need to play out. Hoping for the best for you and me.
Husband is in university of Chicago 177Lu-PSMA-617 trial and has had amazing results. Started in august with 25. Psa and has kept dropping to now 0.25 with no side effects. It does not work if patient doesn’t have pSMA in the bones. We are considering it a miracle drug. Just wanted to put a positive comment on the blog for those of you out of options.
Glad to hear of such a great response. I still think of this as breakthrough treatment, and the FDA designated it that.
Unfortunately, PCa is heterogeneous and complex. My comparative scans showed good concordance (overlap) of PSMA expressing cancer, the other forms that don't express PSMA. There's another level to that, with how well mixed they are on a cellular level. From my results, I'm guessing mixing on the cellular level wasn't good.
I could tell from my clinical signs, treatment associated inflammation which was strongest in the areas that showed highest PSMA expression, and pain going away in those locations about 5 days after treatment, that the therapy was killing some cancer. Unfortunately it wasn't able to get the non -PSMA expressing cells.
Being at this point is strange. I've realized from the beginning that I was in a race with the cancer. It's only been a year since my diagnosis. Since hearing of Lu -PSMA, I was in a race to get that treatment. Unfortunately I was part of statistical 1/3 of patients without good results.
Trials do seem fundamentally different than SOC. SOC at this stage, only buys time, so I see it as a component in keeping me healthy enough to be able to take place in trials. I'm front loading participating in a trial, and not waiting to get to the end if cabazitaxel
Depends on the inclusion criteria. The City of Hope CAR-T doesn't care whether you've had second form of chemotherapy. A lot of trials require it. I'm guessing it has to do with the Internal Review Board ( IRB ).
It makes sense that they would prefer to take patients that have exhausted SOC , since the risk from early trials is unknown. Since you have run out of SOC options the risk versus reward changes.
I guess I need to clarify my statement. I had 6 cycles of docetaxel previously. The CAR-T trial at COH requires at least one prior taxane therapy. Patients don't need to have had two taxane therapies to join the trial.
It just seems that the reports from those here on LU haven’t been very good. I know it is just a small sample but I wish it were a bit better and more hopeful.Car T looks promising although it’s still in early stages. That is what my brother was trying to get to. He was three days from Leukopherisis and had done all of the scans, when he had to be rushed in for emergency spinal surgery. It has knocked him out of the trial.
I know there was a guy on here with the name of Cleodman if you remember, and Car T was what he was trying to get into as well. Unfortunately he had seizures and was enable to do that trial. He was a doctor and had done much research.
Whatever you choose to do, I pray that you have a good response. Please keep us In the loop!
I was so sorry to hear if your brother getting so close, then having his setback. I feel like I'm in a race with the cancer to get to a possible breakthrough trial, while maintaining enough resilience
I think there's a risk of availability bias on the site. It's part of our hueristic thinking to generalize what we see most as being the most prevalent in a broader sense. The vision trial sample of 800 patients is the best place to see the odds.
Yes it did not work for Cleodman the good looking doctor who passed away on March 17 2021, at the age of 47. I think his dear wife still reads and sometimes replies to our posts...Hope it's fun up there......
At the time I scheduled my scan, I had a choice between the two, and chose Axumin for consistency.
Reading your response again,? it sounds like you think FDG might show more cancer, if the cancer has switched from protein to glucose. I'm guessing that cancer needs both for cell function
No. The preferred fuel for prostate cancer is fat. In later stages it switches to glucose. If you want to understand why PSMA therapy failed, you should have an FDG scan. I know it is confusing when you read the ill-informed advice of others on this site. Some know what they are talking about, others don't.
COH has several different CAR-T trials. If FDG is showing discordant tumors, I think only the one targeting stem cells (PSCA) would be useful for you.Arguably, the ones targeting PSMA or PSA might be useful because of antigen spreading. Their BiTE trial that targets STEAP1 may be an option too if IHC shows that your cancer is STEAP1-avid. I'm sure Tanya Dorff can acquaint you with all their trials.
"I usually don't read others' posts, so I can't comment on that. As PCa progresses, it changes from metabolizing proteins (fluciclovine depends on that) and fats (choline and acetate PET depends on that) to metabolizing glucose (FDG depends on that). As you read in my article, cancer cells that express PSMA may not be the same ones that metabolize glucose. There is a shift to PSMA expression that occurs early, and another shift away from PSMA expression that may occur later. So there is an optimum point in PSMA-targeted therapy that may occur. At any given time, there may be some cells that express PSMA, some that don't, some that metabolize glucose, and some that don't. It is heterogenous. Heterogeneity may not be a problem if there is a lot of overlap ("concordant") but may be problematic if there are non-overlapping ("discordant") areas."
Perhaps it was my interpretation of your response that is the problem. Since the heterogeneity composition is unknown, it seemed that it was also unknown which type of scan would best show the extent of the cancer.
It now seems to me that if there's no change in the cancer, two different scans would show both varieties. If there is change then FDG might show more new cancer. I'll ask about switching to FDG from Axumin.
I looked at the PT122 trial on clinicaltrials.gov. It's still recruiting. I do like that it shows an abscopal effect in mouse trials. They put cancer in both thighs, and injected on thigh thigh with PT112. Cancer was attacked by the immune system in the other thigh.
I think I saw an abscopal effect when I got SBRT of the primary tumor during chemotherapy. I had a flare in my hip after each SBRT. When I got PSMA scan a few months later, the cancer in the left hip was dramatically reduced I'm hoping this would bode well for PT112.
BITE and CAR-T both show promise. I'm a little more leery of the side effects of treatment. I hear that CRS is manageable. Leukopheresis and leukodepletion also have risk.
City of Hope has also the AMG 509 trial which does not target PSMA, but STEAP 1. It could be something to consider, since the CART cell trial they have the PSMA 101 target PSMA , the same with the other AMG trial they offer.
Thanks for the information. The CAR-T trial targets PSCA, which is likely a better candidate for me after receiving Lu-PSMA treatment. The first step would be staining my prior biopsy sample to make sure it expresses PSCA.
I'm already partial to PSCA as a target, since it's expressed by all Pca variants.
I thought you were applying for the PSMA 101 trial.
It is difficult to select a clinical trial.. Have you consulted with Dr. Beltran at the Dana Farber or with Rahul Aggarwal at UCSF? They work in advanced cancer and they may have some ideas of possible trials.
I would also consider having a direct biopsy or a liquid biopsy and see if the cancer has new mutations or markers or histology of neuro endocrine PC. Perhaps new mutations may guide selection of experimental therapies.
UCSF might be an option. I'm in Southern California, so a trial on the east coast seems difficult logistically. There seem to be be similar trials at the major centers, often with different brands of similar treatments. Since they are all early phase,there isn't data to choose between them n
Hello, Javelin18! We have already met under your publications, in particular under this healthunlocked.com/advanced... And in general, there in discussions with both me and Tall_Allen, it seemed to me that we discussed all aspects and nuances of treatment with PSMA-617.. I then asked you a number of clarifying questions, but you never answered them..?! Once again! It should be understood that Axumin accumulates equally on the surface of all cancer cells, both PSMA(+) and PSMA(-)! Now imagine that the patient has all the cells in the foci of PSMA(+) or all PSMA(-), and Axumin accumulates on all these cells.. What information will we get from this scan..?? Zero! And on the contrary, on PSMA(+) cells, the FDG molecule does not accumulate at all! In prostate cancer, FDG accumulates exclusively on PSMA cells(-)!In all nuclear centers of excellence, which have been using therapy with PSMA carriers in their clinical practice since 2016, they are aware of several points for which this treatment may not work:
1. Insufficient activity of the Lu isotope at each injection! It must be at least 7.4GBq maximum 10! With mixed therapy maximum: 5 GBq Lu + 5 MBq Ac..
2. The expected therapeutic efficacy of the upcoming treatment by the PET-CT 18F-FDG study has not been evaluated.. It is possible to replace the destroyed PSMA(+) with PSMA(-)!
3. The T level during treatment is higher than the castration values.. It is possible to replace the destroyed PSMA(+) with new PSMA(+)!
4. In the presence of metastases in the bones, drugs for suppressing bone resorption (Xgeva, Zoledronic acid) have not been canceled for the duration of isotope treatment!
To understand why it is necessary to scan with FDG - here are my PET-CT images with PSMA and FDG with a difference of two days:
And this is my picture taken two days later on PET-CT with 18F-FDG.. As we can see, the numerous foci detected with PSMA absolutely do not accumulate the FDG molecule.. My FDG status(-):
Sorry I didn't respond to your previous comments. I'd like to answer your question, but I'm not sure what you are asking. Or are you looking to have a conversation on all the topics in your list?
Yes, my results are really good, I have posted them in the group more than once.. If it's not difficult, I would like to understand for myself: 1. What doses of isotopes were administered to you and at what interval? 2. What was your T during treatment? 3. Did you continue to take anti-bone resorption drugs (Xgeva, Zoledronic acid) during treatment, if you took them at all? Thanks!
No, it can't be that 64GBq with the introduction of such a dose of 177Lu activity, you would die on the spot.. Most likely it is 6.4 GBq..?! But in this case, in the presence of metastases in the bone tissue, this is a very small dose.. Even the standard 7.4GBq with mts in the bones is not enough! Xgeva bone resorption preparations accumulate in bone foci in the same place where PSMA-617 should accumulate.. For this reason, Xgeva must be canceled at least a month before the therapy.. Because these monoclonal antibodies significantly interfere with the expression of PSMA-617 on the surface of cells that are located in the same bone foci.. The standard intervals of administration of 177Lu-PSMA-617 in the centers of excellence with an activity of at least 7.4 GBq is 8-12 weeks! This has been the accumulated experience of advanced centers for years, and I don't understand why those centers that are starting to do this just don't adopt this experience..?! In clinical trials with 177Lu in Russia, the same outrage occurs..(( It seems that within the framework of these clinical studies, these new centers are simply conducting experiments with living people.. How can such a dose of radiation be injected into a person without even evaluating the expected therapeutic effectiveness of the upcoming treatment..?! Sad!
By no means, I am not judging the quality of high-tech medical care that was provided to you! I told you how it goes in the centers that have been engaged in such treatment for several years and drew your attention to the nuances that are mandatory in these centers with this type of treatment.. No more than that!
Okay I'll admit it..... I didn't understand one bit of your posts, but in one of your scans I could see your wallet in your back pocket packed full of rubles.....exchange them for US and the wallet would fit you better.....
I have not heard of denosumab inhibiting PSMA expression in bone Mets. Do you have a research publication on this? Would it also make PSMA PET scans less sensitive and accurate in bone?
I just shared the requirements imposed on my patients by the center of excellence in which I was treated personally. I have not seen any references to such studies. But you interested me in terms of using Xgeva during a PET-CT study with PSMA-11, does this drug affect the accuracy of the examination itself and does it lead to false positive results..?! I will forward these questions to my radiologist from Baku today and report to you on the results of this conversation! Thanks for the question!
I also, like the question about Xgeva, addressed your question to my radiologist in Baku and as soon as I receive an answer from him, I will inform you! P.S. Apparently you made a mistake in the units of measurement of Lutetium activity, MBq or GBq..?!
I'm sorry if I didn't understand you or hurt you in some way! But according to the rules of mathematics 6,975 and 6 975 are not the same number!)) I am also not an expert, but the same patient with the same diagnosis and I thought that we are here helping each other to understand all the subtleties of this treatment..?! You asked - I answered! And no more!
No hurt at all just trying to understand if I should be querying the dosage of Lu-177 I am receiving based on what you are saying should be at least 7.4 GBq.
My provider is giving me an MBq number and I thought your 7.4GBq was the same as 7,400MBq but will check both on conversion of GBq to MBq and my dosage,
I appreciate your input and experience. I will report on what I get today
I don't quite understand the reason for your irritation..?! But if you seriously believe that the questions of other participants and the answers to them under your publication somehow reduces the number of participants who have read your questions in your post, then consider that I have already taken your advice! I'm sorry that I answered these people here, and not in another place!
The Russians have such a saying: "What is written with a pen can't be cut down with an axe!")) And in this case, the problem is not in the head, but in the heart.. After I read about your concern about the results of Lu-PSMA therapy, I tried to understand and suggest to you the reason for this failure.. I am very worried about this! Let's discard emotions and what has already happened and what can't be fixed! Do a PET-CT scan with 18F-FDG and send me a file of this study plus PET-CT studies with PSMA.. - I promise to forward this to a doctor who has been treating isotopes using the PSMA-617 ligand since 2016! I promise that his service will be free for you! I think that if everything is fine with FDG, then you have a chance to go to the second round by adding Ac to Lu.. It's too early to give up, you need to think about what happened and try all the options! 100%
Conversion from “giga” (G) to “mega” (M), regardless of quantity in question (Bq…kg…joules…bits, bytes, etc), is a multiplication of 1000.
Giga is billion, mega is million. So yes 7.4GBg = 7400MBq. In the US we have 7400 = 7,400.
However, some countries (e.g. Spain, France, Norway, the Czech Republic, Denmark) use the comma in the same manner we use a decimal point. So this leads to interpreting 7,400 as equivalent to 7.400 … and that may confuse things.
Again, apologies if I’m misunderstanding the conversation here.
Ah, yes I am in the UK so we use the comma 7,400 MBq or the full stop for 7.4 GBq so yes they mean the same thing here! I had no idea conventions were different !
Finland are presenting my dosage as MBq with no comma or fullstop and i just had 7149 MBq so more than my first dose of 6975 MBq. They do weigh me and take my height..
So I had 7.149GBq yesterday. I'm 5ft 10 inches and standard build.
PSA down to 0.55 pre third Lu-177
PSA since November 2021
Pre-treatment 17.6
25th Nov 2021: 17.6 - Starter Degarelix
10th December 2021: 4.87 - given 1st Lu-177
23rd December 2021: 1.66- Given 2nd Degarelix
14th January 2022: 0.79 - given 2nd Lu-177 and third degarelix
10th February 2022 0.55 - given third and final Lu-177 and fourth degarelix
So not sure what's done what re mix of degarelix and Lu-177 or what my nadir should be given I didn't have an RP or RT . Hopefully yesterdays Lu-177 will pull down further.
At this stage, I can tell you unequivocally that in a Phase III VISION clinical trial on the use of 177Lu-PSMA-617 in patients with metastatic castration-resistant prostate cancer, a scheme of 7.4 GBq of 177Lu isotope activity was used in 4-6 courses every 6 weeks! These studies did not take into account the status of PSMA patients(-)! I would also like to draw attention to the ECOG 0-1 or 2 efficiency status. My opinion is that the figure 7.4GBq is the minimum figure from which to start such treatment! The concept of the emergence of radioresistance has not yet been canceled!
Initial conditions of the Phase III VISION clinical trial
As for me, I asked about the dose but alas forget the answer. My next treatment that question shall be revisited. I'm still on Lupron, so T is very low., not taking Xgeva or Zoledronic acid. Frequency is every 6 weeks for a total of 6 sessions.
Could you expand on this statement:4. In the presence of metastases in the bones, drugs for suppressing bone resorption (Xgeva, Zoledronic acid) have not been canceled for the duration of isotope treatment!
Yes of course! In front of you, the same thing was asked by the participant MateoBeach. I have already forwarded this question to my radiologist in Baku and will share the answer as soon as I receive it!
Thank you. It's a fundamental part of my nature to fight, so I'll keep at it. I'm motivated by the desire to help and protect my family. We have a daughter graduating High School this year. I want to be around to support her in college, and when she starts her career.
Yes, great and inspiring attitude Javelin. Comments by T_A and Nal are spot on, so won’t reiterate. Questions raised by RusLand also worth exploring regarding adequacy of Lu dosing, possibly combining Ac, and the possible impact of Xgeva, which I had not heard about before. Agree with prioritizing Killer T immune trials.
I recently entered a study trial at Dana Farber for LuPSMA617. From my naive understanding, the sponsor, Novartis, is calling the plays. They maybe in charge of dose, frequency, etc. Just a thought.
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
Is anyone familiar with the GUN trial?
Choosing an MO
Keytruda clinical trial
A Quick Update and Trial Questions
