I am monitoring my PSA hoping to delay castrate resistance. My oncologist sort of mentioned a set of rules for defining castrate resistance but i forget the details if i did ever hear them all. Something about three consecutive increases but how much and over how much time and there were other moderating factors.
Is there a concise definition of CR with percentages of rise over time or whatever defines CR?
Castrate-resistant pca (crpc) is defined by disease progression despite androgen-deprivation therapy (adt) and may present as one or any combination of a continuous rise in serum levels of prostate-specific antigen (psa), progression of pre-existing disease, or appearance of new metastases.
Continuous? Appearance of new metastases? How would you know without a series of PSMA or bone or ??? scans? Or is PSA enough to figure it out?
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spencoid2
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Castration resistance is not like being pregnant (either you are or you aren't). It is a process that your androgen receptors go through, and some cells will always be more advanced in the process than others. That said, an increase in the number of metastases on the same imaging test is your best indicator. It has to be the same test - not a new, more sensitive test.
My MO said I was CR when PSA started climbing on Xtandi.... Up 6 consecutive tests and scams shows some activity and CT showed new met not seen on PET scan. NaF18 scan showed same met seen on CT. New met + 6 rises starting small(10-20%) but increased quickly. Last one was up 240% from previous month. Best of luck but don't worry yet..
Simply put it’s the continued growth of PCa despite being at castrate levels of T which is <20. My MO’s use PSA tests to determine this, ultra sensitive PSA test to be exact, since cancer at very low PSA levels may not show up on a scan.
As an example - In order to qualify for Provenge, which requires you to be deemed MCRPC, I needed 2 consecutive rises in PSA, I was metastatic at dx.
Lupron and Taxotere brought my PSA down dramatically. Twelve weeks after my last Taxotere session, my PSA reached a nadir of 1.54, and then started to slowly climb. Seven months after nadir, my PSA had doubled. That was the threshold that got me re-classified as castrate-resistant. and triggered the next layer of treatment. I've had no progression of bone mets or lymph node mets. Oral Zytiga+prednisone and a course of IV Jevtana chemo (I am enrolled in the CHAARTED2 clinical trial) have now brought my PSA down to 0.05, and I hope it stays there for a good long time.
Castrate resistant is when ADT treatments no longer work. Failing one ADT drug does not make you castrate resistant. When you fail several, then you are castrate resistant.
that does not make sense to me. any ADT that does reduce testosterone to very low levels and especially in combination with abaterone or similar would reduce PSA and tumor growth if the PC is still CS. i believe the CR is when there is growth in spite of low T levels.
I was on Abiraterone and my PSA started to rise after a few years. I then went on xtandi and my PSA fell again. Failing Abiraterone did not make me castrate resistant.
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