Initial diagnosis early 2019, PSA at 20. Still before any treatment, nearly a year later, PSA was at 33 early in 2020. (Gleason 3+4, scans showed two probable spinal mets. The mother ship is still intact.)
First medication approach was bicalutamide 150 mg (along with 5 mg finasteride and 10 mg tamoxifen) started early May. Labs at five weeks into the antiandrogen monotherapy showed a PSA drop to 6.4, and three months later (in late Sept. 2020) my PSA had continued dropping, to 3.8. Additionally, ALP had dropped from 152 to 108.
Labs at the next three-month mark (mid Jan. 2021) showed a PSA rise to 23.4 and ALP rise to 267. Stopped the bical immediately, but continued finasteride. We were going to do a four-week bical washout period before starting ADT, but I preferred going six weeks, on the off-chance there might be a delayed antiandrogen withdrawal response and a drop in PSA.
Nope. Got the results a few days ago. In fact, my PSA just rose from under 25 to 185.0, more than a sixfold increase in six weeks! Interestingly, my ALP dropped by 20% to 219. Could this mean the PSA spike is more likely to be coming from the primary tumor, or? Perhaps metastatic activity not in the bones? Just wondering why ALP might drop along with such a massive PSA spike.
Also curious is that six weeks after stopping bical, my T level still remains at the high level (around 1200) that I experienced during the entire six months of bicalutamide. The rise in T was expected and is normal with this drug, but is it normal for it to stay so high for so long after discontinuation? (Prior to therapy, my "normal" T was around 700... all testing done around 9 am on an empty stomach.) What mechanism(s) might explain why it would still be so high?
[Additionally, I decided to try a very-low-protein diet for the past four weeks, after many months of high-protein SAD. Not sure if or how that impacted any of these numbers. Other than low BUN, which could be from that diet, all my numbers were in range. As previously observed, my mild anemia again improved with a worsening PSA.]
So, got only about a half a year out of this med. Hope my mileage is a bit better on ADT!
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noahware
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Sorry to hear that Bicalutamide failed in just 6 months. The pattern indicates that PSA is mainly coming from primary tumor site. Your Nadir PSA with Bical was 3.8 and that was first suspicious figure ,I noticed.
T of 1200 is unusually high even with Bical on board. The strong rise of PSA without rise of ALP is not a bad thing as it indicates that bone mets are not waking up.
As for low protein diet..it does not explain this PSA rise. High amino acids and high fatty acids do cause some increase in cancer cells growth thou.
I hope Lupron/Eligard work well for you. I am continuing with Bical and so far so good. Hoping that spectacular Bical failure does not happen soon.
Consider ADT + docetaxel next. Best results are by alternating chemo and hormonals.
I'm sorry to hear it failed. But its nice that you have backup plans!
Please look at the estrogen patch research and clinical trials. It did wonders for me. Sides were manageable. I don't know how Lupron would have treated me (my bone mass was on the low side and depression runs in my family).
Waiting to hear back from my MO... I already proposed it (with most recent supporting evidence) and he said it sounds "reasonable" but needed to look further into the actual protocol.
I would not use Bicalutamide and keep the prostate. Why didn't you get the prostate treated? Also, Bicalutamide does not work as well as Lupron when there are bone mets.
I would take Bicalutamide after surgery and salvage radiation. But not instead of prostate surgery.
I decided against surgery because of likely mets. So opted for systemic treatment. (Of course, local treatment to primary and/or to mets will be pursued if pain or symptoms suggest it.)
I think bicalutamide does not work as well as Lupron when there are bone mets OR when there are NOT bone mets! It is a weaker, inferior agent. But that is also why the side effects are minimal. So that was the appeal, since some men DO get a good and prolonged response from monotherapy.
If one can add one more drug to the usual succession of progressive drug failures for metastatic disease, why not?
Thanks for the links! Yes, there certainly seems to be growing evidence that debulking the primary can have benefits for metastatic patients. Of course, that was never suggested by any of the MOs, ROs, or urologists I have spoken with (not SOC)!
I admit that I developed an early bias against that approach by reading and listening to those who suggest a surgical removal of the primary may potentially promote metastatic activity, rather than just inhibit it.
I guess both could be true. There are mechanisms to point to and suggest as possible, either way, as a rationale. Unfortunately, not much in the way of evidence at the highest level.
I think removing PCa cells with surgery or radiation makes systemic therapy more effective. This is also the hypothesis of Norton and Simon, here is a slide by Dr. Palma mentioning this:
That hypothesis certainly makes sense when doing something like chemo. If you are trying to kill individual agents of an enemy army with toxins, the smaller the army the lower the amount of toxins needed.
But does it follow for androgen deprivation? You are removing the fuel that MOST of the enemy requires. But whether the overall population of cancer cells is larger or smaller, a certain percentage (that can thrive without that fuel) will remain, and repopulate. I can see, though, how a more significant population reduction could buy a little more time... which is of course the main business of treating metastatic disease.
I think a better hypothesis is that the "mother ship" provides the growth messaging that serves to deploy various factors of production for the distant cancer outposts. An intact mother ship means increased signalling. The counter-hypothesis is that destroying the mother ship might serve to send even greater signalling to those outposts to expand.
I tend to think of cancer not so much as the "army of cells" but as the ideology behind the army. How does killing greater numbers of soldiers impact the ideology, over the long term? Not sure we have a definitive answer.
Noahware...Very interesting style of explaining prostate cancer cells behavior when attacked.
It depends on enemy soldiers capacity and strength. Depriving them of fuel (water supply) can potentially kill all of them irrespective of their size. This is what happens in men whose PSA goes to 0.2 or lower. (very low Nadir) after ADT.
Bicalutamide killed them but did not kill all of them (Nadir PSA was 3.8.) These left over, surviving , cancer cells overpowered bicalutamide and grew furiously giving 185 PSA .
But in many other cases, attacking them too ruthlessly creates a leftover, virulent, Gorilla warfare force( think aggressive variants/NE) and that makes them very resilient and hard to kill. Meaning their ideology and and survival tactics both have hardened. Like ISIS out of Saddam's Republican Army.
I have intuitive feeling that your PCa seems still fully androgen sensitive and Bicalutamide being a weaker drug has not been enough. Your PCa cells churn out a lot of PSA in short time span and therefore, Lupron plus Enzaltumide/Zytiga is likely to work well. Just speculating.
BTW, I will reserve Docetaxyl Chemo for later use as it kills both androgen dependent and androgen Independent cancer cells...(nuclear option)
It's been my understanding that ALL hormone ADT just chases Pca cells while chemo and/or radiation kills them. I'm happy to chase or put the little buggers to sleep for as long as i can, since hormones seem to be less toxic to overall health than chemo poison and radiation burning... which are next-to-last resorts. The ultimate last resort is suicide... not a great option but it does end the cancer. ugh... was a nice day before i let my dark side out. 🥴
I also have a high T (850 before starting Avodart 1100 to 1500 after) but also familial high cholesterol. The Finasteride you took/take does increase T. Also, a doc told me that this is the way statins work. Liver produces T out of C Don't know if this is accurate, as my lab's show the opposite. My T has a weak relation with my residual (after statins that is) C.
ARI inhibitors such as Finasteride ,Dutasteride block testosterone conversion to DiHydro T and this is how T level goes up in blood. Cholesterol itself is raw material for to make testosterone. Besides Bical itself increases T.
Interesting... I knew the bical was raising serum T, but never really thought about the finasteride... of course that makes complete sense, since blocking the conversion of T would seem to mean more is left unconverted.
And although I was taking it for under a year, I also wonder about its potential "masking" effect on my true PSA levels.
Thanks. Do you have reference about what you said about this enzymatic reaction. I would like to know more as I am on 50 mg Bicalutamide monotherapy Intermittently.
If bicalutamide accumulation in cytoplasm of cancer cells is real problem, then.. logically the off period should deplete this accumulation and help maintain good effect longer.
casodex being a hormone, like testosterone, can theoretically feed PCa. Have seen a few studies that claim when it fails, stop using it because it turns into food. I'll go with that if it happens to me.
I would suggest considering starting with Firmagon for your ADT as it will very rapidly take you to castrate level of T without the spikes of Lupron. You can switch over when it is onboard and under control.
It also sounds like you do not know for sure about bone or other mets, unless I missed something. If this is so then I would go for a Ga-PSMA scan to find out. If there were no mets outside of the prostate and pelvis then you might still have a chance at curative treatment by eliminating "the mother ship" (surgery, EBRT, +LDRBrachy) and whole pelvic RT.
Bone scans show what are assumed to be mets. One doc said these can only truly be confirmed as such either via biopsy or via more precise scans. I have been going under the assumption that what the bones scans show is metastatic activity, and that systemic treatment is required.
There seems to still be some debate over costs and benefits of removing the mother ship. Personally, I tend to assume that, when done: a third of the time it is curative and life-prolonging, a third of the time it is too late to prevent metastasis, and a third of the time the removal was not even needed because the cancer was never going to prove lethal. (The latter is perhaps less common, as urologists today no longer seem as intent on removing G 3+3 prostates from 85-year-old men as they once were.)
There are also reports that men who have AR-V7 POSITIVE cancer cells develop resistance to ADT faster than men who have AR-V7 negative Cells. There is a blood test which is used in Latin American countries to know AR-V7 status. In USA, we can know AR-V7 status by CTC liquid biopsy .
I managed to drop my PSA from 20 to 13 in a few months, after being in contact with a man who had far higher PSA (and Gleason 8) and not progressed in several years without any medical intervention, to the surprise of his oncology team. So it wasn't that I did NOTHING, just that I did nothing medical.
The question I asked myself was, how many years longer will I live if I begin treatment immediately versus delaying treatment? I have yet to find a definitive answer, even though the literature suggests SOME survival benefit is likely the sooner one starts on ADT.
Frankly, my first MO was the one who inadvertently discouraged me by posing the treatment progression essentially as this: we will start Med X, and that will fail in a year or two, so we then proceed to Med Y until it also fails, then on to Med Z...
PC itself is USUALLY a decades-long process. The old-school thinking was, don't cut the balls off until symptoms present, because 1) castration also has negative effects, and 2) in the long run, it fails anyway. When I clearly need palliation, off come the balls.
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I felt the fact that I was Gleason 3+4, and not 4+3 or 4+4 or more, gave me a bit of breathing room. Others are perfectly welcome to consider me a fool, but I decided I value treatment-free QoL up front in exchange for a possible shortening of time down the road. Will I regret that? It's entirely possible!
Consider my PSA rose only from 20 to 33 in about a year WITHOUT continuing the dietary/metabolic approach. Had I gone back on that diet (that lowers mTOR, IGF-1, insulin, blood glucose, etc.), might I have been looking at a PSA in the teens rather than in the hundreds today?
When your PSA hit 20 did you have an MRI of your prostate to determine if the cancer was contained? Did you have a CAT scan or a bone scan to determine if it was metastatic at that time?
Factually, an MRI, a CAT scan or a bone scan do not necessarily give you a definitive conclusion of "metastatic" or "nonmetastatic" PC. What they give is evidence of obvious and clinically significant metastases. They only show what they can show.
Having read Anthony Horan and Bob Liebowitz and others, my belief (in line with theirs) is that with a PSA of 20 and a palpable tumor of Gleason 7, the default assumption should be that one already has systemic disease even if the "standard" scans do not show obvious metastases. The cows are in all likelihood already out of the barn. (Hence, the common failure of "cures" to be curative.) That of course does NOT imply that local treatment can not have benefit, even if micro-metastatic activity has been in the works for years.
Yet a PSA of 20 and a palpable tumor of Gleason 7, along with the absence of symptoms, probably also indicates that one is not riddled with metastases and at death's door. With no prior baseline, though, how would I know exactly how aggressive my disease is? One way, since PC is USUALLY a slow-moving disease, would be to watch it and find out.
Obviously, my urologist (and many others) thought I was crazy. Nobody at this stage of disease does A.S. But my plan was for A.S. measured in months, not years. The idea was simply to delay treatment, to see what treatment-free progression would be like. This is obviously not something one would do with other cancers that have MUCH faster doubling times than PC. (When a urologist suggests to G-6 or G-7 men that they need their prostates removed TOMORROW, not next month, he is usually lying.)
And so when PSA subsequently increased, after first dropping, I did the scans later on in 2019. They indicated a low met burden. Because my MO at the time would not entertain anything other than Lupron, and I wanted to do tE2 (or bical), the delay to initial treatment was a bit longer than planned.
For me, the only reason to do scans is if they are going to impact potential treatment decisions. Since I had already decided to delay initial treatment for months, there was no reason to not also delay scans. Same goes for my current situation: regardless of what scans would show, my next move is ADT.
I am not all that worried about taking a little time between my successive progression of treatment failures. My first MO assured me at our first meeting that they would ALL fail, eventually. If someone could convince me in a more compelling manner that rushing from failure to failure would add many years to my life, trust me, I would have been in a full sprint from day one!
I disagree. A PSA of 20 does not necessarily indicate metastasis. Especially a Gleason 3+4. Your lack of action likely caused it to become metastatic. To each their own.
That PC turns from "non-metastatic" into "metastatic" in 6-12 months absent treatment defies everything I have ever read in the scientific literature regarding it being a years-long process. Anthony Horan cites many, many papers regarding the typical doubling time of PC cells and how many years (not months) it takes for them to grow into clinically identifiable tumors, with micro-metastatic activity occurring well before the cancer is usually identified. I would be interested in the sources you are basing your opinion on.
What exactly do you think causes "recurrence" in so many men who are supposedly cured? It is because they had systemic disease all along, when their docs told them they didn't!
You have a logical way of thinking which so much resembles my own thinking in this matter. I rejected heavy duty ADT after 9 months and embarked upon my own milder Intermittent ADT (Casodex+Dutasteride) after reading Dana Farber 2004 paper.I am glad I did this as my side effects almost disappeared and T came back up 500+., Mood, Energy , wellbeing, exercise capacity all skyrocked upwards.
Just like you ..I took a chance with mild ADT with minimum side effects and last 9 months have been very good. Casodex might fail some day...I know..but that day may be far.
. I support the approach you took..yes it was risky ...but a risk taken with full responsibility and awareness.
Ultimate Logic is.. In the end We all DIE....Buying time with best possible quality of life is all that really matter. If Casodex fails...like it did in your case.. I am going to gladly accept next line of treatment. But for now its all roses and sparkles ! Hope it lasts long. Wish me lupron free and chemo free life !
The measurements are secondary to the mechanism of action.
Bical is a blockade that stops testosterone from reaching the Pca cell,
Lupron/Zoladex are androdrgen suppressants which cut off much of the source. These work on Pca cells that are dependant on external testosterone,
Zytiga is one of several drugs that inhibt Pca cells from producing their own (aka the initial castration resistant cells). If Zytiga cost is an issue then research quarter dose Zytiga with a low fat meal (broadly no fried components).
So my read of your numbers is there is a significant castration resistant cell population.
( I was G9, took 11 months to BCR after a radical with clear margins, have a consistent psadt of about 10 weeks and have kept my psa under 2.1 for 5 years, And now am convinced that everyone's cancer experience will vary. )
So in your shoes I would remove the prostate, about 8 weeks latter get a GA68PSMA scan and use SBRT on any residuals if oligeometastatic. (Skip SBRT otherwise).
In the process with SBRT you will have removed all but the circulating resistant Pca cells.
Then reassess Bical/Zoladex/Zytiga or chemo as appropriate for the residual population
I think I tend to agree with LearnAll that my PC is still fully androgen sensitive, because the antiandogen mechanism is not one of castration. If the bical switched from AR antagonist to agonist, then it makes sense that my high levels of T are now resulting in high PSA.
So it will be interesting to see what the PSA response is, when I start actually depriving the body of androgen.
I should have introduced this by saying Root Cause should be the focus. Be it an IT problem, a 737Max crash or a medical issue. Look beyond the numbers, the obvious and delve into the underlying issue.
I tried bic also, in 3 months my psa went from 6,5 to 12.5, was 50mg , found a slight uptake in one met on the side of the vertebre, started with 1000mg of arbitrone and dropped to 1,3 after 10 weeks, I expect another drop to be below 1, hopefully undetectable. Full dosage on a empty tummy one hour before breakfast with 10mg of prednisone, have had no side effects, so far so good and hopefully will get a couple of years or more. It he lowers the dose I will ask him about taking it with a low fat breakfast, would help on the cost, with insurance my share is 351.00 a month, on aarp united Healthcare and will go down once out of pocket puts me in the next bracket. I got it monthly so the oncologist can adjust the dosage if needed, the 90 day was twice as much as the monthly. Also on monthly shots of bone stuff, dumsang , wrong spelling but women take another brand then every 3 months after a year. So far the oncologist had been on the money, feel great, work part time, eat healthy limiting red meat and get the exercise in to combat any fatigue from the meds. Three years into this, chemo back then and Lupton or eligard every 3 months.
Just my thinking about all this so take it for what it's worth. When I started this journey my parents was barely above the cutoff for treating cancer. My uro said that's what cut off numbers are for, I have cancer. A few months later I started 40 ebrt. I had one spot on a vertebra and had a couple shots of the intensive radiation to it. Then I started elegard/lupron for three years. It's been a grulling 5 years but in this situation ya do what ya gotta do. Side effects are awful but you have to be alive to have them. I feel very lucky to have had no treatment failures so far. There are guys on this forum that are geniuses with biochemistry and we are luckier for it. It's reassuring to read that someone else has the same side effects as you. It makes the fatigue and foggy brain more bearable. Never base decisions on what has less bad side effects. Bsse them on what stands the best chance of success. But I haven't so far had to figure out what comes after whatever no longer works and you have. I hope whatever it is works for you for a long time. Mike
I think different people will have subjectively different opinions on the costs and benefits of accepting either side effects of treatments or the potential life extension of treatments. The "right" answer is what is right for each individual.
As one with a history of depression, for example, there is no way I would accept the tradeoff of an extra year of life in return for all my remaining years spent in a deeply depressed state. Would I prefer to live, say, seven years as a free man or to live eight years in a prison cell? Easy choice.
But, ask me again in seven years if I feel the same!
Just another example of how differently people react to treatment. First cancer diagnosis psa 9000 and Mets throughout body. Treatment Casodex, Zoladex, Xgeva and Osteomol. 3 months later psa <0.01. I should mention that I also took vitamins and antioxidants and I crushed 30 apricot kernels a day spread on my cereal. I have no idea if they helped but I persisted for 12 months at the same time the Casodex stopped and I changed to Enzalutamide. I have never had a biopsy or surgery.
Here's an idea. I have been told over and over, for the past six years that "prostate cancer is a heterogeneous disease." That axiom seems pretty well accepted from all the evidence. Assuming this, the prostate has all kinds of cancer cells, from not too bad to really wiley badasses to deal with. If you remove the prostate, all you have left are certain types that metastasized, not the entire variety in the prostate. While the met ones may be able to morph over time, they start out whatever they were when they left the mother ship. Some may be fairly easy to deal with, some harder. But, you only have to deal with a greatly reduced variety. Seems like reducing the range of badasses would be highly beneficial.
I agree that we each have our own cancer, our own response to treatment and our own life experiences. What us great about this forum is knowing that whatever is going on with you, you are always one if the bunch of brothers trying to live as long and as well as we can.
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My Intermittent Bicalutamide mono therapy
PSA rising while ALP continues to drop?
