What if this prevents cancer from becoming resistant?

Posted by denis76 @denis76, Mar 13 2:57pm

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?

Interested in more discussions like this? Go to the Prostate Cancer Support Group.

Profile picture for zzotte @zzotte

@heavyphil it’s always something going on, right now it’s hundreds of medical trials going on I hoping that sooner then later they hit the jackpot

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@zzotte wrote "I'm hoping that sooner than later they hit the jackpot"

The weird thing about hitting the jackpot treating a serious illness is that you might not even realise it at the time. For example, there was no big, magic "Aha!" moment for HIV/AIDS; they just kept tweaking the cocktail of drugs until they noticed that people were living 10, 20, 30+ years. Of course, they didn't know for sure until years later that they had got that right.

I have strong feeling that we're close that same point now with metastatic prostate cancer. Patients are living longer than the lagging SEER data would predict, not because there's a single brilliant cure, but because oncologists have figured out better ways to treat us with what they have (and added a few incrementally-improved drugs into the mix, like the 2nd gen ARSIs). But we won't actually know for many years, when they observe that many of us are (or aren't) still alive.

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Profile picture for northoftheborder @northoftheborder

@zzotte wrote "I'm hoping that sooner than later they hit the jackpot"

The weird thing about hitting the jackpot treating a serious illness is that you might not even realise it at the time. For example, there was no big, magic "Aha!" moment for HIV/AIDS; they just kept tweaking the cocktail of drugs until they noticed that people were living 10, 20, 30+ years. Of course, they didn't know for sure until years later that they had got that right.

I have strong feeling that we're close that same point now with metastatic prostate cancer. Patients are living longer than the lagging SEER data would predict, not because there's a single brilliant cure, but because oncologists have figured out better ways to treat us with what they have (and added a few incrementally-improved drugs into the mix, like the 2nd gen ARSIs). But we won't actually know for many years, when they observe that many of us are (or aren't) still alive.

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@northoftheborder as long they don’t give up I’m in 🙂

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Sorry to join this conversation so late - hopefully I'm not rehashing something already discussed. You might take a look at Bipolar Androgen Therapy (BAT). It kind of approaches the problem of castration resistance using a similar theory. While on ADT with low testosterone, the patient takes periodic testosterone injections. As a result the patients testosterone is constantly cycling up and down. The idea being that cells that have adapted to a low testosterone environment can actually be killed by a sudden influx of testosterone.

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Profile picture for heavyphil @heavyphil

@zzotte This had been around awhile: Bipolar therapy - and as with most late stage cases, it works for some and not for others.
The two completely opposite hormones serve to ‘confuse’ the cancer cells.
That’s my layman’s attempt to explain the biochemistry that is waaaaay over my head!🤔

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@heavyphil I kind of got the gist when he explained to me I felt the same way

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Profile picture for northoftheborder @northoftheborder

@zzotte wrote "I'm hoping that sooner than later they hit the jackpot"

The weird thing about hitting the jackpot treating a serious illness is that you might not even realise it at the time. For example, there was no big, magic "Aha!" moment for HIV/AIDS; they just kept tweaking the cocktail of drugs until they noticed that people were living 10, 20, 30+ years. Of course, they didn't know for sure until years later that they had got that right.

I have strong feeling that we're close that same point now with metastatic prostate cancer. Patients are living longer than the lagging SEER data would predict, not because there's a single brilliant cure, but because oncologists have figured out better ways to treat us with what they have (and added a few incrementally-improved drugs into the mix, like the 2nd gen ARSIs). But we won't actually know for many years, when they observe that many of us are (or aren't) still alive.

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