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What if this prevents cancer from becoming resistant?
I saw a thread about half-dose medications.
Guys, what do you think about whether resistance can be avoided? Read below.
Another option is to use different combinations of ADT and lutamide. For example, one month is ADT without lutamide, the second month is ADT with lutamide, the third month is lutamide without ADT, the fourth month is neither ADT nor lutamide, and then the cycle starts over again, so as not to repeat the previous cycle (the combinations would be reversed).
I had this thought, perhaps it's naive, but for some reason my intuition told me exactly this. What do you think?
In other words, varying the medications is necessary to avoid resistance. I've heard of guys who are still alive for 30 years; maybe they did exactly this?
I voiced this thought to my oncologist, and he said it wouldn't work with high Glyson levels.
At that moment, I thought about resistance as cancer adapting to low testosterone levels. The cells change and no longer respond to low testosterone.
And if you really want to "let the cancer swing," you can try to keep testosterone levels fluctuating rather than staying steady, and change the ADT + Lutamide combination depending on PSA growth. For example, if PSA growth is significant, ADT + Lutamide is taken for a month; if PSA growth is moderate, Lutamide alone is taken; if PSA growth is low, ADT alone is taken; and if PSA growth is not observed, the duration of Lutamide-only treatment is extended (2 months instead of 1 month). In any case, the method is based on the fact that we don't "create" a wall for the cancer, but rather a swing when it doesn't have time to adapt (testosterone levels fluctuate, but we don't allow it to fully utilize them with the help of lutamide).
I want to try this on myself, but fear holds me back. But who knows, maybe this method works.
Why do I think this method might work for those with a PSA level of almost 0 and whose cells have not yet become resistant to cancer?
Argument 1: If cells are still dependent on testosterone, they will respond to ADT and lutamide when drug therapy is resumed.
Argument 2: By changing combinations and increasing testosterone levels, we prevent cancer from becoming resistant because we are changing the "rules of the game" and not dealing with cells that are no longer responsive to ADT and lutamide.
Argument 3: By repeating combinations in a cycle (ADT and lutamide, ADT only, lutamide only), we maintain a basic level of protection by closely monitoring PSA levels, which is an indicator that resistance is not developing.
Argument 4: Cancer has little time to "start firing." A new combination will either lower testosterone (ADT) or dampen the ignition.
Argument 5: It's no secret that they're making money off us, and the higher the stage, the more money they make. But they can make much more money if resistance develops (medicine is a business), and perhaps that's why ADT and lutamide inevitably lead to the development of resistance! What if we take our luck by the balls and say no to a society in which someone profits by keeping silent about the easy way out (when registration doesn't occur)
And finally, if the cancer becomes resistant, then we're done for, and we need to avoid it at all costs to keep the cells sensitive to hormones.
What do you think, guys? Is it risky?
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@denis76
Your testosterone will barely rise after three months. It might not even get to 50. It will probably take a year to get it back to even low normal
The fact that you are on Erleada will delay the time it takes to become a castrate resistant. There’s at least one person in this forum that is in a clinical trial testing that.
If you stay on Erleada And your PSA starts rising without ADT you have added a second problem, that you have become hormone resistant to Erleada. I stopped ADT for eight months while I was on only Nubeqa. My testosterone rose to 50, But my PSA stayed undetectable the whole time. Did you look into that trial that includes ADT with Erleada?
I became castrate resistant after 2 1/2 years when I was only on ADT. It’s been six years since then, and I’ve had no problems keeping my PSA undetectable, I am on Orgovyx and Nubeqa.
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5 Reactions@denis76 Intermittent hormone therapy was validated by the Embark study. Our oncologist suggested we read it because he is suggesting it for my husband who is Gleason 9, oligometastatic in his lymph nodes, and PSA is down to .04 on Orgovyx and Nubeqa. The results of the Embark study are promising!
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3 Reactions@ucla2025
I don’t know if I would call that intermittent Hormone therapy. They did not recommend stopping and starting ADT on a regular basis.
According to the studyWhen somebody had a PSA hit < .2 at 36 months they would recommend stopping the treatments. All drugs not just ADT. They then reinstated it when Prostatectomy patient hit greater than .2 and radiation treatment treatments patients PSA was greater than or equal to 5.
This actually isn’t that revolutionary. A lot of doctors will recommend their patients stop drug treatment to see what happens when their PSA becomes undetectable for a year or so.
This article discusses the exact details.
https://dailynews.ascopubs.org/do/embark-real-world-practical-tips-using-enzalutamide-high-risk-biochemical-recurrence
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4 Reactions@jeffmarc The article says that EMBARK reestablishes the role of intermittent hormone therapy. I suppose individual results would determine if it was beneficial to stop and start on a regular basis. I watched an interview with Dr. Freedland talking about using intermittent therapy with patients and how their QOL was much better with the intermittent therapy. Thanks for your comment.
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2 Reactions@ucla2025
If you read further down in the article, the intermittent Hormone therapy is after three years and stopping all drugs. Nowhere in that study did they mention stopping just ADT and starting it back up again randomly. They stopped it after three years and restarted it when PSA hit certain levels.
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4 Reactions@jeffmarc In my mind stopping and then starting again when PSA rises is “intermittent”. At least that’s how our oncology doc explained it. Doesn’t sound like a random stop and start to me if it’s based on keeping close track of PSA. In any case, I’m grateful for their work. Our doc said the intermittent use of the drugs is becoming more popular.
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2 Reactions@ucla2025
Waiting three years to do it is not intermittent. Waiting a year to do it and then watching the PSA could be intermittent. I think with the person that initially asked about this was asking is if they could just stop and start ADT at random intervals, that doesn’t fit with the embark trial.
@ucla2025 These are EMBARK's conclusions:
❝In patients with prostate cancer with high-risk biochemical recurrence, enzalutamide plus leuprolide was superior to leuprolide alone with respect to metastasis-free survival; enzalutamide monotherapy was also superior to leuprolide alone. ❞
In other words, Xtandi alone was better than Lupron alone, but both together gave the best results. They didn't test stopping both.
https://www.nejm.org/doi/full/10.1056/NEJMoa2303974
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1 Reaction@jeffmarc Thank you Jeff, I understand now.
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2 ReactionsYes, guys, thank you very much for the information, and a special thanks to Jeff.
Two main questions.
1. If the PSA has dropped to zero, how long should it take (six months, a year, or more) before trying to wean off ADT?
2. Does testosterone deficiency (ADT) cause resistance. How long should I stop it and monitor my PSA monthly?
My calculations may be incorrect.
Regarding 1.
It depends on the speed at which the PSA dropped to zero (in my case, it took almost a year and a half to drop to zero). If it takes a long time, we wait longer and then stop ADT.
Regarding 2.
I believe it depends on the extent of the lesion before treatment, the initial PSA, and the Gleason score. The higher the PSA, the higher the Gleason score, the shorter the break period. For example, for those with a Gleason score of 9, the break should last six months (at this point, you should try to increase testosterone by any means necessary), while for those with a medium/low Gleason score, the break can last one year.
And another thing: question two depends on the testosterone growth rate. If it grows faster (in younger patients), then the break period can be shorter.
In other words, the main variable is the rate of testosterone growth, so that the cells "recognize" its presence and don't transform.
I'll discuss this with my doctor and post the results here.
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