I have castration resistant prostate cancer with a Testosterone level of 6.
I am not sure why I am still taking Lupron when it is clearly not working? Ideas?
Like everyone, I hate the side effects! Thanks in advance!
History: Diagnosed at Stage 4 (2 years + 3 months ago). Reached mCRPC 1 year ago. First therapy: Docetaxel with Lupron, then just Lupron for 1 year, 4months. Then added Abiraterone for 8 months. Currently stopping Abiraterone and I am having EBRT on femur. In three weeks I begin Radium 223.
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baltha
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It IS working. It is suppressing your testosterone. As castration resistance occurs, the androgen receptor multiplies on the cancer cell surface. That makes it even more sensitive to even the tiniest amount of testosterone. It is more important than ever to prevent any testosterone.
As I said, it's already super-sensitive to testosterone.
BAT is highly experimental.The TRANSFORMER trial showed that BAT can help in some cases, but may make it worse. It should not be done outside of a clinical trial.
Lupron isn't working - in the sense of controling your PCa - even though you remain castrate. So it's a fair question.
The therapeutic target of Lupron is the androgen receptor [AR] axis. Quite often, when castrate resistance occurs, the AR axis continues to be the target & Abiraterone or Enzatutamide, for example, is added to classic ADT (e.g. Lupron).
You are coming off Abi, however, so it's reasonable to ask why, then, is it important to remain on Lupron? If your CRPC is getting all the androgen it needs, it does seem pointless.
A few studies have tried testosterone replacement, which is effective for a while in a minority of men at the CRPC stage. The idea being to reverse CRPC & restarting ADT. Other studies have tried DES (diethylstilbestrol), which does more than cause castration. It too works for some for a while. In both cases Luprom would be halted.
& then there is BAT (bipolar androgen therapy), where men swing from super-high T to castration in short cycles. Because of the long wash-out time for Lupron, men using Lupron remain on it throughout. I am currently on a modified BAT & use oral DES, which can be stopped for the week that T is high. (I do not have CRPC at this point, however.)
The European Association of Urology (EAU) guideline, the American Urological Association (AUA) & the National Comprehensive Cancer Network (NCCN) all mention the need to maintain ADT when CRPC develops.
"Despite consistent guidance to maintain backbone ADT in CRPC, there is a wide variation in actual clinical practice. Cross-sectional survey data from 3,477 patients with CRPC in five countries (France, Germany, Italy, Spain and the UK) revealed that between 19% and 45% (in the UK and Italy, respectively) of patients received chemotherapy alone with no ADT"
Hello, I will repeat what my oncologist told me when I asked him the same question. Prostate cancer is heterogenous not homogenous. There are many different types. When the PCa is still in the prostate gland it is treatable. When it escapes the prostate gland and metastasizes (usually to the bone) the horses are out of the barn. The PCa horses are not the same colour. There are white horses, black horses, brown horses, palominos and everything in between. Your luperon drugs might still be effective against one type of PCa cell. If you stop it, you are back to square one. To quote my doc again, he said you are on the ADT train. With metastatic cancer you are on that train for life. You might add various drugs to your train and you might take one or two drugs off your train but you stay on the train for your entire journey. Hope that helps!
There are some regimens under exploration to restore some androgen sensitivity. Most well known is a round on taxane chemotherapy. That is why it is usually alternated between advanced AR drugs. Niclosamide plus bicalutamide has been shown to restore enzalutamide sensitivity.
Apalutamide with Abi may be superior to Xanti by inhibiting AR proliferation.
BAT in some form or schedule may work well by disadvantaging the different AR cell type sub populations ( colors of horses) by alternating high T with castrate T periods.
I like and have been following BAT as I think it's interesting. I think it may be helpful if even for making the PCa hormone sensitive again. The on/off, low/high modulation in therapy to trick or fluctuate the effectiveness in the cellular function of prostate cancer seems intuitive. Rather than the all/none, use till it stops working modality. I wonder then too, if shorter courses of treatments and switching between them, might keep the cellular process confused enough that it couldn't build a resistance, etc. There's some interesting aspects to this.
On a simple comparative level, I think it's like weight training with free weights. Muscles become programmed and workouts must be changed over time, tissue must be confused and not kept in a particular format, because gains are then harder and harder to realize. The muscles adjust to the resistance and movements (memory) over time doing the same thing, the same way. When changed, they respond as if starting anew. Anyways...
Well... That's just my overactive mind thinking too much while wading through the deep weeded pond! Lol
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