So, at the end of August 2020, a personal curator, a nice, friendly employee of the center, meets me at the airport, who gives me a local SIM card with an Internet package connected for free and takes me to the hotel that I pre-booked through Booking. The next morning, I arrive at the center to meet with the head of the center, Dr. Fuad Novruzov, to take blood tests and undergo PET/CT with 18F-FDG. A CD with a recording of my recent (no older than 2 months!) PET/I brought a CT with 68Ga – PSMA with me. In the preliminary approvals for my treatment at this center, I was also warned that I should stop taking anti-bone resorption drugs (Xgeva, Zoledronic acid, etc.) at least a month before the expected date of PSMA therapy. Also, I was advised to continue ADT in order to keep my Testosterone at castration values. Let me remind you that, by that time, I had not taken any antiandrogens.
Dr. Novruzov explained to me that somehow anti-bone resorption drugs mask cancer cells in the bone tissue and that is why they should be stopped for the duration of isotope treatment. Later, I found confirmation of his words when I independently familiarized myself with the criteria for admission of volunteers to the I-phase of research with the therapeutic drug 225Ac – PSMA-617, which Novartis started. There was also talk about the cancellation of anti-bone resorption drugs at least two weeks before participating in these trials.
The doctor also told me that the study on PET/CT scans with FDG are performed to assess the expected therapeutic effectiveness of the upcoming treatment by imaging the localization of foci that do not accumulate the PSMA ligand - these are prostate cancer cells that do not have PSMA protein on their surface, but, nevertheless, attract the FDG molecule (FDG(+)/PSMA(-)). In this center there is a special computer program developed by specialists of the Cancer Institute in Heidelberg, into which the files of two PET studies are uploaded/CT with PSMA and FDG, and the computer itself gives results about the accumulation and localization of these two diagnostic RFPs, and their ratio in specific foci. Further, the radiologist makes an assessment of the expected therapeutic efficacy of treatment using the PSMA ligand as a percentage. For example, in the presence of FDG(+) to PSMA(+) in evenly mixed foci in a ratio of 50% or more in favor of the former, the expected therapeutic efficacy tends to 0%. Moreover, such therapy is contraindicated in such patients due to the risk of avalanche-like replacement of radiation-destroyed PSMA(+) cells with FDG(+)/PSMA(-) prostate cancer cells with a sharp increase in PSA levels within a short period of time. This is important to understand! There are also variants when in one focus FDG(+) and PSMA(+) cells are localized in colonies that practically do not intersect with each other. Sometimes there may be separate, independent foci in the patient's body, both with a PSMA(+) pool of cells and with a FDG(+) pool of cells. In a particular case, PSMA therapy may be justified, due to the fact that the destruction of foci exclusively with a pool of PSMA(+) cells will not lead to their replacement by FDG(+) cells that are located in another independent focus.
Later, in some studies, I found confirmation that the study on PET/CT with FDG is of no small importance as a criterion for selecting patients for radioligand therapy using the PSMA ligand. In particular, randomized phase II studies TheraP concluded: "Lower response rates to PSA were observed in men with FDG-PET MTV 200 ml or higher (38%) than in men with FDG-PET MTV less than 200 ml (56%).). After adjustment for randomized treatment, the probability of a response to PSA was significantly lower in patients whose MTV FDG-PET was 200 ml or higher, compared with patients whose MTV FDG-PET was less than 200 mL (OR 0.44, 95% CI 0.23-0.84, adjusted P = 0.035)." Another study also talks about the importance of understanding the patient's status for diagnostic rfp 18F-FDG before starting therapy using the PSMA ligand: ncbi.nlm.nih.gov/pmc/articl...
But back to my story. According to the results of a PET/CT study with 18F – FDG, no foci of pathological accumulation of this rfp were detected in my body, despite the fact that according to the results of a PET scan with 68Ga - PSMA, I had multiple foci in the bones of the skeleton, in single regional lymph nodes and in the primary focus in the prostate itself. SUVmax in some of them reached 198.0.. This meant that the malignant cells in my foci express a lot of PSMA protein on their surfaces, which is the target for radioligand therapy using the antibody PSMA-617. The expected therapeutic effectiveness of the upcoming treatment was estimated as more than 90% success rate.
Further, taking into account the fact that with this therapy, a large load falls on the kidneys to remove radioactive waste from the body along with urine, liver and kidney blood samples were analyzed and kidney scintigraphy for SPECT was performed. Also, according to a general blood test, the hematopoietic functions of my bone marrow were evaluated. All these tests and studies I had were within normal limits. And the attending radiologist decided on the possibility of conducting therapy for me according to a tandem scheme using two therapeutic RFPs 177Lu – PSMA-617 and 225Ac – PSMA-617 with a short interval of administration, with doses of isotope activity of 5 GBq and 4 MBq, respectively, for the first course of therapy, and then according to dynamics.
From that moment on, I was ready as an astronaut to fly into space...))
To be continued, follow my publications!
P.S. I deliberately divided my publication into several parts of two A4 pages of typewritten text with font size No. 12. I think that longer texts with information that require comprehension should be assimilated for the reason that while you finish reading such a text to the end, you already forget about what was in the beginning ..))
VISION trial results of Lu-177-PSMA-617
Overview of 177Lu PSMA trials
Radium-223 and [177Lu]Lu-PSMA
