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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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@grandpun
Thank you for your response.
In the age of capitalism, when people make money off sick people, I think this is pointless.
The main risk is resistance; it's the point of no return. Many of us, including myself, have no choice.
I already stated my arguments in the opening message.
In my opinion, statistical data processing is needed for those who survived.
I graduated from university and know what mathematical statistics is. I may be wrong, but my main assumption is that resistant cells are much more dangerous than cells that haven't yet become resistant.
Challenge #1: Identifying significant influencing factors rather than variables
Challenge #2: How to test assumptions over a long period of time
Challenge #3: How to develop assessment criteria and a response to changing dynamics (accurately assess how cancer responds and predict its behavior)
I believe that while our cells are hormone-dependent, there's a chance (metastases don't invade vital organs), but once they become resistant, all we can do is fight their growth, with almost no chance. In other words, wasting time is like shooting ourselves in the knee.
If our PSA is almost 0, then there are few cells and they're not yet resistant, but if the cells don't respond, there's no turning back.
Any risk must be considered in terms of probability and its proper assessment.
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1 Reaction@denis76
Becoming castrate resistant is not a fatal problem, At least not fatal For most of us because of the drugs that are available.
I became castrate resistant six years ago. Zytiga and Nubeqa have allowed me to stay alive for all this time. Yes, it’s better if this doesn’t happen, but the drugs that are available do work to keep us alive.
As for doctors profiting off the drugs. Yes, if you’re going to a urologist that’s not part of a big complex and they’re giving you ADT injections They are definitely making a profit off of that. The same may be true of other cancer doctors that work independently.
If you are treated at a center of excellence or Have Medicare advantage the doctors don’t benefit in any way from the drugs you’re taking?. Their medical systems might even want to limit the number of people that get some drugs because the expensive ones may not be completely reimbursed. The doctors get a salary that is not affected by the drugs that are Prescribed.
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4 Reactions@denis76
Gleason 8
Starting PSA 54.0
Metastasis to seminal vesicles an other suspected metastasis within the pelvic cavity
@jeffmarc
Jeff, please remind me. How long did the cancer last before it became resistant? Were you taking lutamide before that?
@ededed
Wow, Dear Friend, could you please write in more detail? Was your prostate removed? How many years ago? What was your PSA trend? What are you taking besides ADT, lutamide, or other medications? Are you active (sports, sex) or passive (less exercise, no sex)? Could you please describe in more detail what happened after the biopsy? I think many people would be interested! Thank you!
I think you and I are on the same page. I have Gleason 9 and I'm thinking about trying a combination of these, but I'm still afraid.
4 years without ADT?
@denis76
In 2010 I had my prostatectomy 3.5 years later had the salvage radiation I got 2.5 more years before I started Lupron, in 2017. It took 2 1/2 years before I became castrate resistant.. So it was more than 9 1/2 years after I was diagnosed that I became castrate resistant. At that point, I went on Casodex for a little over a year and then abiraterone For 2.5 years. Then I went on Nubeqa Which I’ve been on for almost 3 years and undetectable for 28 months.
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2 Reactions@jeffmarc Jeff so they decided not to give you ADT at the time of recurrence. Did they know where the recurrence was? Was that the standard of care at the time, or something you requested? Obviously, you are doing well, but I may be facing slavage and wondered whether if they can't identify the PSA source, one should just wait post radiation and watch PSA or do ADT with radiation?
@dhasper
They did give me a 6 Month Lupron shot two months before I had the radiation. Just a one time thing didn’t have it again for five years.
They did the radiation because my PSA hit .2 3.5 years after The prostatectomy. I did meet with the radiation oncologist before they did it, and they explained the reason why they wanted to do it. That was 2014 so the best they could do was a CT scan to see if anything was found. Like most people who have PSMA PET scans under this condition, Nothing is found so savage radiation was done.
Latest trials have shown that the ADT is more effective if given at the time of radiation or after it, rather than two months before. Doctors aren’t really paying attention to this yet.
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1 Reactionhttps://www.pcf.org/could-more-testosterone-be-the-hidden-key-to-fighting-prostate-cancer-part1/