Patrick wrote today that when we start ADT the “ clock starts ticking .” I’ve been reading stuff for 14 years so I trust his opinions . Now I also have respect for Tall Allen after a few months on this wonderful website. If I understood him correctly I think he cited a study recently showing that “early “ use of systemic therapy did not hasten the onset of CRPC . ( I can’t remember how the study was structured. )
After 10 years on Avodart ( plus diet and many other off label drugs and supplements ) to treat my Gleason 6 PCa , I stopped Avodart for one month 2 years ago . My PSA doubled . A return to Avodart did not stop its rise . It got to 61 before I got a PSMA -PET in July and radiation 6 weeks ago . MSK docs say STAMPEDE trial indicates 2 yrs ADT and Zytiga for me .
Interested in everyone’s thoughts . Thanks in advance .
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You have high risk localized PC, may be micro metastatic (PSMA PET/CTs do not detect anything smaller than 4 mm). The local treatment may take care of the cancer in the pelvis and the ADT plus Zytiga of the micro metastasis if they exist. After the 2 years you could stop the ADT and Zytiga, let the testosterone go up and see what happens. Hopefully you are cured. But wait to see what the people you trust tell you. .
It usually takes longer than 2 years of ADT for the cancer to become castration resistant. If the cancer ends up being metastatic the use of abiraterone along with ADT will delay the cancer to become castration resistant and will improve overall survival.
There is not way to know for sure for you at this time. The very high PSA is worrisome and time will tell.
I believed the Stampede trial demonstrated a 30% or so reduction in castration resistance after 2 years of adt + zytiga...its most likely the median time to progressions was so much better. And that was for metastatic men.
It is not up to "everyone's thoughts." Patrick and other persons on this site have made such erroneous claims before. If it were true, they would have evidence for it (and by evidence, I mean something beyond the mouse studies that Patrick draws his knowledge from).
We do not have a complete picture of the "natural history" of prostate cancer, but we do know that castration resistance is a multifactorial process. Here's the evidence (from humans, not mice):
Some patients (and doctors) believe that by delaying ADT, they can increase their quality of life, and delay castration resistance. Neither is true. Contrary to popular belief, decreasing the intensity of hormone therapy and delaying its use brings earlier castration resistance and death. The strongest evidence for this comes from the STAMPEDE (on Zytiga and Xtandi), LATITUDE, and SPARTAN trials. Among men who were newly diagnosed with metastatic prostate cancer:
•Overall survival was longer if men used Zytiga + ADT.
- No difference based on the number of metastases
- Failure-free survival was longer if they used Zytiga + ADT
• Overall survival was longer if men used Xtandi+ADT
- Survival was especially lengthened if there were fewer metastases
- PSA progression-free survival was longer if they used Xtandi+ADT
• Overall survival was longer if men used Erleada+ADT
- PSA progression-free survival was longer if they used Erleada+ADT
A clear pattern emerges: early use of intensive hormone therapy prolongs survival and prolongs the time to castration resistance.Men who were oligometastatic benefited from early, intense hormone therapy.
The TROG 03.04 RADAR trial examined the duration of hormone therapy in high-risk men treated with radiation. They found that, after 10 years of follow-up, men treated with 18 months of ADT survived longer, and reached castration resistance later compared to men treated with 6 months of ADT.
The TOAD trial looked at starting ADT at the first sign of recurrence vs. waiting for metastases to be detected. Men treated earlier reached castration resistance later. It also showed there was no major detriment to global health-related quality of life by starting ADT earlier.
Maha Hussain reported the results of a randomized clinical trial comparing intermittent vs continuous ADT in recurrent men with metastases. She found that:
• Time to castration resistance was not different for the two protocols (Figure S5)
• For men with minimal disease, overall survival was 6.9 years for those on continuous therapy vs 5.4 years for those on intermittent therapy. The trial was underpowered for this difference to reach statistical significance.
• It took 4-5 years for the survival curves to start separating - long follow-up is needed to detect survival differences.
Taken together, all these major randomized clinical trials show that the best way to use ADT in the oligometastatic setting is to use it early and heavily. Reducing the number of cancer cells as quickly and effectively as possible, even reducing those cells that haven't begun to measurably contribute to PSA, extends survival. The effect of evolutionary selection pressure allowing castration-resistant cells to survive is dwarfed by the reduction in sheer numbers.
TA, you state that “Reducing the number of cancer cells as quickly and effectively as possible…extends survival.” But if I understand you correctly, you are not a fan of radiation for oligometastatic APC (along the lines of “can’t hurt, but won’t help” prolong survival). Could you please clarify? Thanks.
I think his position is if the cancer is beyond oligometastatic; more than a few metastases, radiation doesn’t help. Palliative RT of course if there is pain. I think
My position for the oligometastatic situation is - I don't know if metastasis directed therapy helps. Just as picking off a truffle from under an oak tree has no impact on the enormous plant (the mycelium) that extends throughout the soil and into the roots of the tree, I don't know if picking off a few of the largest visible metastases has any impact. I do, however, know that systemic treatment has a major impact.
I like your ability to get to the heart of the questions. If I understand correctly non met pca is not indicated for Zytiga but is for Nubeqa. In my case after one month on Nubeqa my psa was undetectable. Monthly Lupron for a year before PSA doubled in my 6th yr of pca.Or do I read wrong?
That is true that Nubeqa, Erleada, and Xtandi are indicated for non-metastatic CRPC. Zytiga should be too, but I guess they never requested the indication from the FDA.
my hubby has non-metastatic Pca; dx Jan 2021 and had 1 injection of Firmagon in Jan., then started Eilgard on 3-month cycle--now slightly more than 1 year of ADT. ALSO on Zytiga, but did not start that right away--never suggested until we visited a 2nd MO who ordered Zytiga--we were both hesitant because everything says it's for metastatic, but we listened to reasoning by Tall_Allen and a few others. Hubby says he feels better on Zytiga, but I think it's the prednisone :)His PSA 2 weeks ago was 0.06 (down from 0.17 in Dec.), but his T is creeping up. The lowest T has been was 24 in Sept., then 37 in Nov. and now 54--don't really understand this, but glad we decided to go with the Zytiga even though non-met.
I recently recently completed 2+ years of ADT + zytiga. I think it cannot be underestimated how important it is to drive the psa to 0. The main difference is this was my first round of ADT. It's still too early to know for sure if ADT + 2nd line adt prolongs time to crpca but I think the clinical trials are pointing in that direction. More importantly, I think it's very important to keep the beast under control to be able to take advantage of the newer treatments in the pipeline. And there are plenty. When I was diagnoses in mid 2019 my MO actually was reading the latest Stampede results prior to my appt. He told me the committee that discuss the treatment plans thought it was the right treatment for me. They weren't sure if the insurance would cover it. The insurance approved and the rest is history. There are many members who have been treated similarly with great results. No reason to think you'll be any different.
Thanks very much . That’s very reassuring ! Tall Allen’s response above covers all the bases .
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Is zero a reasonable goal? As in 0.00. Or is it something else for people that received radiation and not surgery?
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There are many other men on this site who have had RT along with ADT + 2nd line adt treatment. Their psa tests are undetectable. I use 0 as the lower limit but I believe everyone understands that is the technically possible. ADT will lower prostate psa in addition to prostate cancer psa.
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I see from your profile that your PSA seems to have nadired at <.04. Is there a significance to that number, hence the < sign?
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The < means undetectable. My psa level is lower than the testing equipment can detect...in other words undetectable. Technically, it's impossible to have zero psa because other tissues besides the prostate produce psa however it's so miniscule that it's never considered.
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Well, ultra sensitive tests can get into the thousandths, more specifically designed for post-prostatectomy, and in fact .03 or above has been noted as a marker for BCR in post-prostatectomy. So I just wondered if there was a industry standard so to speak, to consider <.04 as undetectable in radiation cases and is it the goal to stay there. I’ve been getting <.1 results but I wonder why they don’t do more sensitive in RT cases. Hopefully I’m not hijacking a thread
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I've been getting my test done at Quest from the very beginning with a few Lab Corp results sprinkled in when tests were conducted by the hospital. .I don't have it listed but one Lab Corp test came back < 0.01 so I can only assume that my psa is less < 0.03. The only purpose for ultrasensitive psa is post RP. After that, there is no reason to get an ultrasensitive psa test. What possible treatment decision would be made if a psa rose from .007 to .009?
The sensitivity of the PSA test needed depends on the nadir, but usually no treatment decisions are made unless PSA rises above PSMA detections limits of ~0.5-1.0+. So if the nadir is less than that, it could be considered superfluous information. I did RT with HDR-BT/IMRT/ADT and doing uPSA tests. Nadir was <.02 on ADT, and one year after stopping ADT hovers around 0.04.
I took a test of my own from Ulta, a Beckman PSA test, that was meant for post-prostatectomy patients, even though i had whole pelvic and prostate EBRT (as well as a scapula that had an indeterminate blip) and three months out from my last one month shot it said .03. Not < or > just .03. Which to me sounded pretty good but considering my T, which I also tested for, was up to 74 from 7, I really wasn’t sure what to make of it. Will it go up as T goes up? Is there any prognostic value from the number at all? Its not .02 so that means something is still there.
I use Ulta through Quest, and believe the lower-limit in my report is <0.02. As your T goes up, it will indicate if you have any prostate material left-- some of which could be benign, and some of which could be hormone-sensitive (HS) PCa. If it were to track linearly with T, it would likely be benign, whereas if it were to track exponentially with T, it would likely be HS PCa (and have a doubling-time of less than 1 yr). My T went from <12 to 700, and PSA went from <0.02 to and average of 0.04 for the last year, indicating it's probably benign tissue.
My hubby was dx with high risk, aggressive, stage 4 Pca in Jan. 2021. He was put on ADT right away and had 8 weeks of Proton therapy; a couple of months after the proton, he started Zytiga. PSA and T were steadily going down, then had a blip in both after starting Zytiga; however, PSA is 0.06 as of 2/8/2022 but T is going up. Lowest T was 24 in Sept., then increased by 1.5 times to 37 in Nov. and now 1.5 times again to 54 in Feb. I thought the increase in T was due to Quercetin he had started so we discontinued that,I thought I understood about T but obviously I do not. I have been concerned about the rise, but 1 of 2 MO's says he doesn't care about T. WHY NOT? The other tests regularly for T levels and even mentioned if it keeps going up, might need to put hubby on something else--didn't say what
Not sure I understand what you mean in your explanation above about T rising.
I know Zytiga is supposed to stop androgen production; I also read that anti-androgens (Zytiga is not) work by blocking the AR receptor and allowing for more circulating Testosterone. Perhaps the Quercetin WAS acting like an anti-androgen and blocking AR receptors, thus increasing circulating T?????
Anyhow, could you perhaps explain more about inc. T levels? you said yous has risen to 700 but you don't seem concerned.
Hi KA, I believe Zytiga blocks T at the AR, while Lupron suppresses T at the testicles, and at a greater magnitude. So if your husband’s T is rising, perhaps too much is still being produced. Should he also be on Lupron? While on ADT, it’s desired to be at castrate level (<12 in my case), so your MO should monitor that. I’m 18 months post-ADT, so T should be rising back to normal ~700.
I had no SE's from BT, other than the first two weeks, a little urgency. It's been 2 1/2 years now, no delayed toxicity like proctitis, bleeding, etc. Had a good doctor for BT-- Chang at UCLA. For ADT, I did Lupron for 18 months, and Zytiga for the first 6 months. I stopped Zytiga due to high BP, but Lupron drove PSA to <0.01 anyway. ADT was relatively easy for the first year, typical SE's, muscle fatigue and hot flashes. But after year one, SE's seemed to accumulate into more severe form like joint pain and muscle loss. I exercise a lot, and eat well, and that helped a lot. PSA was <0.01 for a the last year on ADT, so I decided to quit at 18 months instead of going to 2 years.
Not all pc patients express psma. 20% of them do not express psma. I am not sure if I missed reading this but a psa of 61 with no psma Mets are not completely non metastatic
I’m currently planning to do the 2 years of ADT and Zytiga because I agree that the clean PSMA -PET does not mean no mets. And PSA 61 is troubling . I have been thinking all along about the microscopic ones that the scan can’t see . I forgot that some PCa cells don’t produce PSMA. Thanx for the reminder .
I had the same thing but couldn't get a better scan approved 2.5 years ago so same treatment with bone/ct scans and a PSA of 156/90/110 before the start of ADT. Off all treatment for now, next PSA test 3/15.
TA cites an important paper above where "Maha Hussain reported the results of a randomized clinical trial comparing intermittent vs continuous ADT in recurrent men with metastases. "Here a link to that study:nejm.org/doi/full/10.1056/N...
Some men might find it interesting to scroll down to Fig. 3, click on it, and examine the two survival curves (A. Minimal Disease, and B. Extensive Disease) and really think about what the graphs are telling you viscerally, rather than in statistical lingo.
We see in both curves that men in both groups start dying in year one. Oddly, the men with extensive disease getting iADT (in curve B) continue dying at a SLOWER pace than the cADT right up to year five! Now, their better survival is not "statistically significant" here, but the fact is that more than half the men in BOTH groups are already dead and the better median survival is in the iADT arm, by half a year.
Am I claiming men in the iADT have better early survival than those in cADT just BECAUSE they are getting iADT? Of course not. The curves are too close, and by the time you get to year nine the few survivors in that group start dropping like flies, anyway. What the curve says to ME is "hey, if you have extensive disease, there's about a 70% chance you'll be alive after 3 years and about a 70% chance you'll be dead after 8 years, no matter which of these two treatments you choose.... if you hope to live a lot longer, it looks like cADT might be better to get you there." What does the curve say to YOU?
Likewise, take a look at curve A, Minimal Disease: at about three years, you really start to see an apparent benefit to doing cADT. (Of course about a third of the men in both groups are already dead by now, so not much benefit to them.) But oddly, at eight years, the curves come back together. After that point, when about 60% of the men in both groups are dead, if you were part of the lucky 40% there doesn't seem to be much disadvantage being an iADT guy... the iADT seems to help get the "luckier guys" to year 8, 9, 10, 11 and 12 just as well as cADT.
From the statistical perspective, you are only allowed to take away from these curves what the math and rules tell you: for example, that "For men with minimal disease, overall MEDIAN survival was 6.9 years for those on continuous therapy vs 5.4 years for those on intermittent therapy."
Note that TA left out the word "median" in his post above, which is perfectly fine from a statistical perspective, because that is how a term like "overall survival" is defined. But a layman might interpret the sentence to mean, wow, I get an extra year and 1/2 by choosing this therapy. Well, yes, you do, if you happen to be in a study and die right at the point of time where half the men were dead and half the men were alive. Most men, by definition, do NOT die there... they die sooner, or they die later, and may not see the same benefit of a particular therapy as implied by the study.
This is in no way a claim that the information TA provided above is not correct, helpful or useful. It is ALL of that, and I (like most here) appreciate his input on this forum immensely and would go so far as to say he is literally a "life-saver." I am just trying to provide a perspective on how the graphs in studies might speak to us when we look at them directly, rather than when we try to understand them in statistical terms that many (like myself) do not intuitively understand.
Unfortunately, the only point TA was making with referencing that study is there is no difference between iADT and cADT. TA specifically states the study was under powered. His point, from my reading, is there is no evidence showing iADT yields better results, as some claim on this site. The risk is greater for selecting resistant strains when doing iADT than cADT which is why the multi modal treatments are having profoundly superior results.ALAS, as with most things in life, too many make pca the center of their existence and spend too much time study ways to better the best clinical trials. A fools errand in my opinion.
" His point, from my reading, is there is no evidence showing iADT yields better results..."
In which case his inclusion of the fact that for men with MINIMAL disease "overall survival was 6.9 years for those on continuous therapy vs 5.4 years for those on intermittent therapy" would be somewhat superfluous to the point, as well implying to some that iADT is inferior. And my point is, that sentence about "survival" may not mean what some think it means, and that may become more apparent when the actual survival curves are examined and considered.
I am not making any claim that the evidence here is showing iADT yields better results. I am making the claim some men may be curious and interested in looking at the actual survival curves within studies, as they tell a story of what is happening to individual men within the different groups, over time. They tell that story better than statistical jargon, except for those that can think well in terms of statistics.
At some point before median overall survival is reached, men in the iADT group might have been saying, wow, we are dying off faster than those guys... guess we picked the wrong therapy. But for a few years AFTER that point, they could look at the dramatic change in slope of THEIR survival curve and say, wow, we are now dying off at a lower rate than those guys... guess we picked the RIGHT therapy. (This would apply only to the men still alive, as presumably the dead ones would not be talking to themselves.) Later still, the few surviving men in both groups might look at each other, shrug, and say "I guess THAT choice (of iADT or cADT) wasn't a deal-breaker... what do you think kept us survivors alive so long, if it wasn't our decision to choose one or the other of those two therapies?"
From the point of longer term overall survival, what that study appears to show is that it probably doesn't make a huge difference whether you choose iADT or cADT. (Looking at the curves, one might better wonder, what helps one end up in the 30% of both groups that all survive well past the others, versus ending up in the 30% of both groups that all die before the others?)
What the study DOES say is that "intermittent therapy resulted in small improvements in quality of life."
And yes, major randomized clinical trials show that the best way to use ADT in the oligometastatic setting is to use it early and heavily. But wouldn't some of us want to know, too, if they show that later (after treatment failure) survival and progression are always improved by continued and endless maximal suppression or "anhiliation" of androgens? The Gatenby trials on adaptive therapy have brought that supposition into question, and have pointed out that what is commonly referred to as "iADT" has always been applied under rather arbitrary standards for PSA thresholds and timing of on/off cycles, rather than by using the mathematical models of evolutionary population ecology and tailoring them to an individual's PSA dynamics (and other factors).
This is not advice on how a patient should proceed. It's just a suggestion that we are still learning how to optimize and personalize treatments, with a hope to reduce treatment resistance. Of course, some people think that being curious and reading about these theories is foolish, because they are not currently applicable with anything approaching clinical certainty. By no means should anyone learn anything or think about cancer research OTHER than what clinical trials reveal... your time should be spent on "better" activities, LOL. (Kinda makes me wonder why those others waste so much precious time on internet forums, themselves!)
I hope PBnative has checked out of this thread and is on his way to getting the treatment recommended to him by MSK and digested the reply of TA so he can get on with his life.
I think he like many of us are interested in best treatment but the constant over analysis, life revolving around questioning research and speculation is a distraction from enjoying the time we have left here.
I guess this is how you want to spend the time you have left on earth. That's your call.
Not sure it is helping anyone here though. It will be the real scientists and phase 3 RCT's that leave a mark on the future.
I'm not trying to be rude either. I worry about you. But then I am no saint either. I have my obsessions and addictions too. Just different than yours.
That's very kind of you. I was starting to wonder. But be gentle, because as another forum member has informed us, I lack a certain level of... well, "emotional capacity." Guess I forgot to top off the tank, dammit!
To assert that "questioning research and speculation" is a distraction from enjoying the time we have left would be to assert that what other people might enjoy, or not enjoy, can be objectively determined by you. That is a quite a trick, because I always thought that what a person "enjoys" could only be subjectively determined by that person!
It is also curious how a few minutes, or hours, spent on a forum defines that one's "life is revolving around" that activity. I suppose it is, in the moment. But I am about to go outside and stack some wood, and spend more time doing that than this. Presumably, because you are not with me, you will be unaware that, truly, "my life resolves around stacking wood" even more so than it does around a pointless over-analysis of PC studies. And what a waste of time, stacking wood, as it is (objectively?) such a distraction from enjoying the time we have left here! Perhaps I will bump into a little birdie out there, who can set me straight.
Internet forums are great places... filled with people who can tell you how you ought to spend your time. So many mommies and daddies... and here THEY are, wasting precious time by taking time to tell me I'm wasting precious time!
See, the thing is, I started my post saying "some men may be interested..." I think it's implicit that some men may NOT be. The solution? Just. Stop. Reading.
It is not incumbent upon you to tell me YOU are uninterested, or that you don't think anyone else should be, or that by reading further PBnative will somehow NOT be on his way to getting treatment and getting on with his life.
I am not telling anybody they SHOULD read my posts, or SHOULD look at the survival curves within studies or they should NOT look at them, anymore that I would suggest they go out and start working on a collection of Standing Liberty quarters, or they shouldn't. (Isn't coin-collecting also a waste of time?) I find the survival curves fascinating. Poor me.
Likewise, I am not telling anybody they SHOULD be understanding "median overall survival" as a term is used within studies or they should NOT understand it. But if Daryl wants me off this site on account of my intensely high use of letters, spaces and punctuation marks, that's certainly his call. In the meantime, all anyone needs to do when posting a thread "Interested in everyone’s thoughts" is amend it with "Interested in everyone’s thoughts, except Noahware's." I will oblige all requests!
Internet forums are great places... filled with people who can tell you how you ought to spend your time. So many mommies and daddies... and here THEY are, wasting precious time by taking time to tell me I'm wasting precious time!
This a highlight also:
To assert that "questioning research and speculation" is a distraction from enjoying the time we have left would be to assert that what other people might enjoy, or not enjoy, can be objectively determined by you. That is a quite a trick, because I always thought that what a person "enjoys" could only be subjectively determined by that person!
Yea the thought crossed my mind this guy is pretty intelligent he probably just spends an hour or two every couple days immersing.
Aside from my physical limitations stacking wood sounds good.
I'm on the way to the basement work bench to assemble some printing press assemblies. Then ....ship it! Then...invoice it !
When is there ever a better time in our life for us as individuals after stage 4 dx to spend time however we wish.
Yes. An advanced pca patient should not waste their time reading a study that yhe authors themselves state is inconclusive due to the low number of events. It is my opinion to read what others are doing and the actual results they are getting. For example, of I was new to this site I would know that adt+ zytiga is superior to mono Casodex by a country mile. I would learn it's not wise to convince my MO to try a half-assed attempt at a clinical trial that hasnot released treatment results yet. I would ask what the latest stage III clinical trials show and which one best fits my condition.
And I would do this all the while lifting weights and doing cardio at my gym. Now that's constructive.
And obviously, we SHOULD all have the same opinions that you have, and we should all do what "you would do." Bro, wouldn't your gym get a little crowded?
Everybody on the planet knows adt+ zytiga is statistically superior in clinical effect to mono Casodex, including me. Where have I ever suggested otherwise?
And why are you calling my MO and the Dana Farber oncologists half-assed? After all, he willingly prescribed the protocol without hesitation, and his colleagues were the ones writing the Lancet editorial deeming it "an appropriate form of ADT" well BEFORE we began it. [Dana Farber will NOT do BAT, for example, because that IS still considered "experimental" by them.]
If you have an issue with Dana Farber "experimenting" on patients, don't you have a duty to bring that to people's attention, perhaps with a stand-alone post condemning their policies and procedures? I mean, helping other guys is what you're all about, right? Better sound the alarm!
[Please, don't forget to warn all the men about Lupron, which has the exact same 7% failure rate as tE2 to get men to castrate levels in 3 months. You service to others is needed there, too!]
You seem to want to keep attacking me for "experimenting on myself" with tE2. In fact, I did no such thing: it was prescribed for me by a leading and respected MO whose institution had just deemed it "an appropriate form of ADT."
Since obviously your only interest in participating on this forum is "to help others" I would suggest you apply your concern about others doing self-experiment to those who have done that well before conclusive safety and castration-efficacy results of the PATCH trial had been reported. I mean, I'm just a low-level guy, a follower... you need to do a take-down and expose the Big Guy who was the original self-experimenter, who had so many men follow his example and experiment on THEMselves.
His name is Richard Wassersug. Your duty is to save men from him. Take him down. (And hey, don't forget the personal attacks on his character, exercise habits, and "emotional capacity" while you're doing it.)
I'm attempting to save you from yourself. You are not Dr. Wasserman nor are you under his care.
Turning my attention back to you...what studies are you using that show single arm ADT yielded the same or superior results that ADT + 2nd line treatment for men with bone metastases?
As for my half-assed comment, that has nothing to do with your "Dana-Farber" MOs. You are the one who stated you were looking for a MO who would do ADT via estrogen. It doesn't shock me a MO obliged. Afterall it can be a legitimate ADT protocol but not for you. You should have been on ADT + Zytiga since day 31..first 30 would be Casodex.
You are now, most likely in the mcrpc group. A group that my MO told me is a game changer that coincided with his facial expression. I'm sure your MO is of the same opinion. It's time to put away the pubmed. Whatever benefit you may have received will be of little help in your current situation.
Just reading some old threads coming up on searches and wanted to comment on your reply.
I know several people that lost loved ones to cancer including my Mother losing her Dad to Lung Cancer. In discussions I've had with multiple survivors it hasn't been uncommon to hear that they regretted their loved one chose to continue therapies with serious side effects at a late stage in the disease which may have extended their life for who know how long but they were pretty miserable on the treatment.
Having said that, in looking at well over a hundred studies one thing kept popping into my head was that the difference in time to Prostate Cancer Specific Mortality between treatment compared to no treatment was smaller than I would except or hope in many cases, especially in the context of an average lifespan. Granted I have not talked to a survivor of a loved one with Prostate Cancer which is one of the relatively slower progressing cancers.
My point is facing mortality it a tough proposition and Medical Oncologists are basically tasked with the primary objective of keeping you alive. I think human psychology makes us predisposed to getting "lost in the numbers." Treatment routes are highly personal decisions but they should be based on achieving one's personal target for a balance of quality of remaining life versus life extension.
The things that I keep trying to stress on this forum in that everyone's cancer is different and everyone responds differently to treatments.
There's nothing you can do about the first part of this. However, when it comes to treatments, if it's working, stay the course. I am not a fan of treatment vacations. You are only giving new cancer cell lines a chance to find a work around. Every time I hear someone on this forum say their doctor is scheduling a month or year of an ADT drug, my response is why the time limit? How does a doctor know how long a drug will be effective?
You seem to respond well to treatment, so don't limit yourself with any drug. You might do very well with zytiga.
Little Johnny walks into drugstore and asks for a box of Tampax. The druggist asks "is it for Mommy?" No he replies! "For your Sister?" Once again No he replies! So the druggist asks "Who is it for?" So Johnny replies: It's for me, I saw on TV that you can run with it, swim with it, ride with it and even dance with it !!!!!
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