It looks as if my Lu-PSMA treatment isn’t working. I’ll post more on that when I have the energy. I have my second PSMA scan on Wednesday, and had my third Lu-PSMA treatment last Friday.
The question I have for my my doctors is whether the binding of LU-PSMA to the cancer would prevent binding of the Ga PSMA tracer to the cancer, giving an inaccurate reading of PSMA expression.
Doctors are researching and discussing, but I’d like opinions from the group about whether the scan will be useful this close to treatment.
Written by
Javelin18
To view profiles and participate in discussions please or .
Great advice. I’m on that path now. I have appointments with Dr Shen, UCLA research department, Dr Dorff, City of Hope, this week. I also requested an appointment with Dr Aparicio, MD Anderson. Definitely flying into the unknown now.
That’s a long discussion that I’d also like to have with the group, but for now trying to get some data from Lu-Psma scan. I think there are two steps, figure out if current treatment is effective, then figure out what to do next.
The Lu-177 kills the cell. Dead cells are cleared away quickly. If you want to understand the reason the therapy is not working, ask for an FDG PET scan.
Thanks. When scans are discussed on the forum, I'm sensing the opinion is FDG is much better than Axumin. In my reading of the posts I hear an undercurrent saying that Axumin isn't useful for comparison. I'm trying to figure out why that is.
It seems to me that the quality of the interpretation of a scan depends on the skill of the radiologist. Both Axumin and FDG show more diffuse signatures than PSMA, and require interpretation. Both can be used in comparison to PSMA scan to show non-PSMA.
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.
You could discuss having an Axumin PET/CT which is more specific for prostate cancer than a FDG PET/CT and it is also independent of the presence of .PSMA in the mets.
What is your indication that it isn't working? Two treatments might not be enough to tell. I did an FDG scan a month after my second treatment that showed that there was more work to be done, and I continued on. My PSA was low and relatively stable however.
Prior to treatment, my PSA was 101, and ALP 189. As of one week ago, PSA 183,,ALP 494. Because of that, they moved my PSA scan from end of February to beginning.
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.
18F-DCFPyL PSMA PET/CT for Lu-177 eligibility evaluation
LU PSMA
Six cycles of Lu-177 treatment
Favorable Ga-PSMA scan results at UCLA !!
