We meet with my spouses oncologist on Tuesday. Bill has been on lupron solid for 6 years now. He has had Provenge, Xtandi, Dosetaxel, Cabazitaxel and all worked for a good time, but his PSA has been steadily and firmly rising and new bone Mets for the past few months. My question is that since the cancer has already found a way around the hormone deprivation, what would be the harm of discontinuing the lupron?
What are your thoughts?
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NWLiving
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One of the reasons why castration resistance occurs is because the cancer multiplies the androgen receptor. This makes the cancer super-sensitive to even the smallest bit of testosterone. So it is more important than ever before that he continues to take Lupron.
Not a doc. No idea just why but MY UO stated today I would be on Lupron for "life". It was the only treatment available to me at DX. Been about 3yrs now with 11mos of Xtandi added.PSA Starting to go back up and discussion is about what will replace the Xtandi when PSA moves from single digits maybe into teens and twenties while retaining the Lupron/Eligard.
Guess its cause the cancer is even sensitive to testosterone than it was before. So for most it’s lupron for life. Oh joy🥳. Hope the next treatment goes well.
The PCa "industrial complex" continues to be fixated on the androgen receptor [AR] axis. While Lupron resistance invariably occurs, it is not associated with a rising testosterone. i.e. Lupron, as a castration drug, continues to "work". The cancer has simply become castrate-resistant [CRPC].
After 6 years on Lupron, Bill's testosterone [T] might not recover if Lupron were to be stopped. In any case, recovery takes many months. If he has run through all of the AR axis-related drugs, you might want to investigate Dr. Sam Denmeade's BAT studies involving men with CRPC [1]. The idea is simple enough. If CRPC has adapted to low levels of T, how might they react to restoration of T at very high levels?
A certain percentage of men see a significant PSA reduction. However, recognize that heavily-treated men cover an array of treatment-induced adaptations.
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On a similar note, Diethylstilbestrol [DES] has occassionally been used on men with CRPC.
"In contemporary studies of DES as an agent for ADT in D2.5 patients, a reasonable response rate (40% to 60%) of modest duration (5 to 8 months) is noted." [2]
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And Bill could switch from Lupron to DES while on BAT.
I am currently using DES & BAT. The clotting risk of DES can be dealt with via D-dimer tests & Nattokinase, IMO.
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