I am trying to get an idea of better test labs markers besides just the usual PSA for becoming castrat resistant, because if my SOC of ADT (Orgovyx, and Nubeqa) is starting to fail I would want to immediately jump on BAT.
My doc always adds LDH.
Conclusion: Our analysis suggested the association between a higher level of LDH and poorer OS and PFS in patients with mPCa. As a parameter that can be conveniently evaluated, the LDH levels should be included as a valuable biomarker in the management of mPCa.
The current theory of the prostate cancer stem cell (PCSC) may help us understand cancer recurrence and treatment failure of prostate cancer, and CD133 is one of the most powerful biomarkers to identify and isolate PCSCs. However, the PCSC theory is still a subject of conjecture in some aspects, and the value of CD133 in PCSC or other cancer stem cells was challenged by some conflicting data. The primary aim of this review is to summarize the recent research progress of CD133 in PCSC, including its selective expression in undifferentiated cells, its correlation to treatment resistance, its gene regulation and functional analysis, and its targeted therapy in vitro, in vivo, and in clinical trials. Further elucidating the detailed mechanism of how CD133 is involved in the maintenance stemness properties, will be beneficial in developing effective PCSC-specific therapy targeting CD133.
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KocoPr
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Good thoughts, KocoPr. However, any trial for mCRPC only patients is going to require CR established by standard criteria of rising PSA while on castrate (T <50).
My question for myself was: why wait for CR to try BAT when it is possible some form of BAT might be able to delay or prevent CR from developing? That is why some others, and myself, are using mBAT while still hormone sensitive. If one stays on continuous ADT long enough CR will develop.
Im leaning towards doing BAT, but in also not doing SOC presently as you know i am also doing Osterine and cardarine. Osterine seems to also inhibit PCa, but know definitive evidence yet. Im reluctant to change things up just yet as i am only 6 months on Orgovyx and Nubeqa and having no side effects. All liver numbers are normal, PSA of course undetectable, T less than <5. Estrodiol E2 normal. Only thing RBC and hemoglobin slightly low.
The other thing is i need to get a better handle on the BAT drugs and Cycles like when to take this drug and how much, when to get off that drug, when to change cycles and then i can hopefully convince my OC.
There is no need to get earlier detection of castration resistance because you would continue current therapy anyway until either PSA rises to 2.0 or is very rapid or scans show new metastases.
Thanks TA. I know that is the present doctrine, but so was watchful waiting and then active surveillance until as in my case until tumor escape. Why wait for an outcome that is much worse in magnitude. 2.0 PSA ?
It is an unmet need between HSPC and CSPC.
Maybe one could say i need to try something else Doc now that my CSC markers ie CD133 or LDH are increasing along with a very low PSA numbers increases like 0.05 to 0.08 to 0.10 etc.
Doc how about I get on this trial or can i get early treatment on AKR1C3 inhibitor, Or BAT.
I would think the system could do better than just waiting for a bad situation to get worse.
ALP alkaline phosphatase is included in the CMP and is a marker for bone formation which in turn indicates bone deformation which can be PCa spreading. However ALP is also a marker for trouble in the liver so I prefer testing bone-specific ALP, BALP. On one occasion when I tested both they went in opposite directions, modestly.
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Does taking Zytiga slow down becoming Castrate Resistant?
90 years old, castrated resistant prostate cancer w PSA 20
When your PSA start raising up is that means your castrate resistant? 
Is it useful to get a PSMA-PET scan with low volume cancer, newly castration resistant and PSA below 1?
