My PSA has edged up from 2 to 3.6 while on Lupron and Abiraterone/prednisone. I had a PSMA scan that showed the primary relevant finding as:
- ‘Increase in size and radiotracer uptake of PSMA avid sclerotic lesions in the left lower iliac bone. This is concerning for progression of osseous metastatic disease’
It also showed:
- ‘Interval improvement of radiotracer uptake in sclerotic lesion in the left proximal femur’
I’m thinking this is pretty hard evidence that the Abi is failing and I’ll need to move on to other treatment(s). Details are in my profile but my prior treatments have been Lupron, Abi/prednisone, and RT.
I have a MO appt on Monday to discuss things and I’d like to get some feedback on treatment sequencing before then. I’m thinking it will be:
- Xtandi
- docetaxel
- Xofigo (since I only have bone mets)
- Pluvicto
I assume I’ll remain on Lupron throughout.
Does this seem reasonable? Any combinations? I know this is all high level and there may very well be other factors that pop up but it helps me if I have some sort of hypothetical plan in mind.
Thanks
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fireandice123
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I'm not a doctor. I scanned your bio and did not see initial staging info (ie, was it intermediate or advanced?, gleason #'s, decipher score?, family history of PCa?, etc...).
I did see you stopped ADT a couple of times. Why did you do that? When you did stop, was that lupron alone, lupron + abiraterone, or what exactly? Were restarts driven by PSA rises alone?
Have you had chemo? If not, was that your call due to FOSE (fear of side effects)? Did ADT cause especially difficult SE's?
I am off ADT+Abi myself now, but that was due to my MO's suggesting I could after 21 months of undetectable PSA on ADT+Abi.
Was your PSA undetectable all the while on ADT/Abi?
Just because you had radiation once doesn't mean you can't again, You can have SBRT many times. Of course you mention other forms of radiation as well. I would talk to a radiation oncologist about possibilities of bone being radiated with SBRT.You and I were diagnosed at same time, same age, had similar numbers,metastatic cancer, I never had it in bone so that may have let me take a different path in our treatment.
I have followed a find and kill with SBRT approach which has been very effective. I've avoided ADT only on it for two years, RP, IMRT to whole pelvis prostate bed, and nothing else only two SBRT session 3 days each.
Currently very low STABLE PSA. My plan to continue as I have in the past stay off ADT at all costs if possible. Hope I remain stable for ...
I see KWON at MAYO in Rochester MN, this approach to not working towards castrate resistance by being off ADT has worked very well for me. I say this for others who may read this concerning their choices.
You have to become an expert in your PC and your possibilities.
So I originally was on ADT with IMRT for whole pelvic and prostate bed that was part of the plan with Kwon. I was on Lupron for two years, a year and 1/2 based on Clinical trials probably would have been sufficient as well. So that was first pass with radiation. Now moving forward I expressed my interest in being off ADT. ADT masks what the radiation actually has done, how successful it has been. This was Kwon's original plan for me for SBRT without ADT.
He later also suggested i could be on ADT as well. I said I want to see what the radiation does, I don't want to be on ADT for a number of reasons including I did not want to hasten castrate resistance.
Kwon and my radiation oncologist are both supporting my SBRT radiation without ADT.
I also see other doctor(s) at other cancer hospitals. They support MAYO/Kwon running my care.
My story continues, where it goes from here like all Metastatic PC has not been determined. I get ultra sensitive PSA tests monthly/ bimonthly depending on circumstances, I get scans to see the results from radiation.
I am hearing great enthusiasm from my caregivers about my results todate. I feel I am doing the things that will give me the greatest chance in my fight.
Incidentally I went across the country to UCLA to participate in the clinical trial as one of two hundred patients that lead directly to a PSMA scan being approved by the FDA. I also participated in a MAYO clinical trial comparing PSMA vs Choline.
There are now doctors that believe that with recent advances PC is becoming a disease that men will be able to live with, and no longer resulting in death.
So to continue on your ADT inquiry.
One other national cancer center I have gone to does a variation of intermittent ADT. So they look for specific PSA levels to determine when to stop and when to start back up. This isn't time dependent, it is PSA levels dependent. I will consider that and consider what I drugs or procedures I might use to suppress testosterone if that becomes necessary, or what to use to block testosterone's bonding to PC.
The goal is to live a long life, unaffected as much as possible by treatments. Keep castrate resistance away. To try to be alive for the treatments coming that will extend life or cure PC. To die with or without PC, not from it.
That's very similar to the sequencing that my oncologist in San Diego is recommending. I'm at the point where Xtandi is failing and docetaxel is next on the list.
Some trials are looking at combining enzalutamide with chemotherapy or even Pluvicto earlier in treatment.
Docetaxel + Xofigo is generally avoided due to marrow toxicity.
Enzalutamide + Lu-177 has some emerging data but isn’t widely used yet.
Staying on Lupron?
Yes, you'll likely remain on Lupron (or any ADT) indefinitely, as it continues to suppress baseline testosterone levels, even if other treatments are layered in.
Your plan is solid, and it will be interesting to hear your MO’s perspective. You might also ask about circulating tumor DNA (ctDNA) testing or genomic profiling to guide sequencing, especially if considering PARP inhibitors (e.g., olaparib) or trials.
That is one possibility though I’m not technically oligometastic. At last count before the last PSMA scan I had 7 separate mets though all in the same area. I’ll be meeting with my RO as well.
The number of mets associated with oligometastic PC is Not fixed. The term was invented by Dr Kwon at MAYO. Originally he chose three, then five, this number may increase and increase as experience is obtained.I has 5 nets to begin with, all were killed by IMRT, later a lymph node showed up, it was hit by SBRT at that same time another was predicted to appear at a specific spot, it later did and that was hit with SBRT. So seven to date and I'm current at a low STABLE PSA.
I understand your recent PSMA scan used the radio tracer PILARIFY detecting cancer smaller than 3mm. Do you know what the smallest detection threshold is? Why not Tx. The detected Mets with any of the tools available ie. HF Ultrasound, SBRT, cryotherapy etc?
2mm detection has been possible with scanning in the Netherlands for years. They have been considered to have the best capability in the world. I think it was with an advanced MRI.
More info would help: G score at initial diagnosis, Stage after recent testing to start.Are you being treated by a urologist or a medical oncologist skilled in PCA?
I am on Lupron/Nubea again after 10 month vacation from all med per two MO suggestions. Initial diagnosis 2015, G9, aggressive, local, RT including HDR, stage 2c.
Recent psma scan no cancer in prostate but spot on L2 treated with radiation. PSA now 0.08. Stage IV.
I think I'm in the same track a year (or more, hopefully) behind you. I finished the 2.5 years ADT then after restoring T my PSA went over 2.0 in 10 months. Recent scan shows several lymph node with cancer so their first step is back on ADT until it fails. I'm told it WILL eventually fail just a question of when.
Why wasn't the first choice to attack the PC possibly with SBRT. Or several other choices such as cryotherapy, or surgery, or combinations of these? I would talk to MAYO.
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