As I am 10 months PSA undetectable and clear on basic bone scans I have started the process of consultation re staying on ADT (zoladex) and Apalutamide continuously or moving to intermittent (and what would that involve) or getting more treatment (J591 for example aimed at micromets).
Following consult with Finland onco yesterday his letter says:
'Hormone Therapy is not curative. B's disease has already been treated much more actively than generally has been the practice in ref studies.
Continuous hormone treatment also increases the risk of castrate resistant disease. My experience is that it is possible to pause both chemical castration and apalutamide with the PSA and testosterone being monitored. PSA could increase slowly as testosterone recovers and any sign of disease progression will cause a re evaluation.
I recommend starting the antiandrogen bicalutamide 150mg x 1 for 6 months from July 23 followed by a 6 month pause and again 6 month treatment.
A new baseline PET-CT is recommended after ADT and Apalutamide is stopped'.
I think some of that is controversial and its the first suggestion of bicalutamide.
Seeing my London MO next week but had my April injection last week and have my apalutamide ongoing.
I had numerous bone mets in Dec 21, am tolerating the drugs (still working )
Happy for all views/ experiences
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Brysonal
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So you will have done “full” ADT for 12 months (in addition to your other treatments) before going on 6 months bicalutamide then a vacation. A tricky one and perhaps not unreasonable. Did you discuss doing a further 6 months “full “ ADT before moving to bicalutamide and whether, in his opinion, this would materially increase the risk of developing castrate resistance? I certainly found 6 months use of bicalutamide plus CyberKnife was ok for buying time and some on here have adapted it for “adaptive “ therapy which may be worth you considering since you have thrown the kitchen sink at it. Good luck with your decision and congrats again on your excellent response so far
My London Oncologist has written a slightly contradictory letter to my GP stating he would support my move to Intermittent hormone therapy but would prefer I did another 12 months on the double I am on atm. Due to have a face to face next week so will hopefully find out what intermittent would look like for him and his views on bicalutamide.
I may just have my July inhjection but nice to know I may have an option!
I remember that but you should organise a better injection service.
They should use the original needle and they should rotate the site of the injection and they should avoid giving the injection into the scar tissue from the previous injection and they should do the injection slowly and deep into the fat tissue without rupturing the derma.
Was the injection site warm for extended time and did you develop high temperature?
Thanks for sharing. I also found interesting the bicalutamide suggestion. I'm also scheduled to stop treatments this month after 12 mo ADT+Nubeqa, docetaxel and SBRT to address BCR and probable small met to C5 vertebrae. Have been <.01 for about 10 months. Not expecting a cure, but longer remission and QoL.
I previously thought about "stepping" down to something like bicalutamide to keep my testosterone relatively in check (not castrate, but not raging teenager again either). My One didn't recommend it -said it's best to just stop, be healthy with T again, and if things come back they want to see and treat it again. Not entirely sure what to think, but many studies seem to suggest iADT isn't inferior to continuous ADT while QoL will be higher. We'll see, but that's my current plan anyways.
Hope things go well and let us know what your London team has to say.
‘We had a discussion about whether B should at some stage stop his hormone therapy. For patients with metastatic disease, intermittent hormone therapy is an accepted treatment, having only minor, if any, inferiority in terms of survival compared to continuous endocrine treatment. The quality of life is of course very much better.
B’s hope is that when he stops endocrine therapy there will be no later rise in the PSA. Even though this is an unlikely outcome, I don’t think he will come to much harm in trying it. The question is, what would be the best duration of treatment to produce the survival benefit seen with adjuvant hormone treatments? For locally advanced (non-metastatic) prostate cancer, three years of ADT (eg Zoladex) has been shown to prolong survival. The addition of an androgen receptor targeted agent (ARTA) (apalutamide-like drugs) for two years has caused further survival benefit.
B has been on ADT for 16 months and an ARTA for 8 months. He is thinking of stopping treatment in June this year. I think I would encourage him to continue for a further 12 months beyond that. We will discuss this further in the future.
His plasma PSA remains undetectable. I have prescribed a further 2 months of apalutamide for now and will review him again at the end of April’
My London MO is a good guy, SOC type who has tolerated my ‘add ins’ of early Lu-177, 2x brachytherapy’s ( he wasn’t happy with this) and a further SBRT than the UK would have done. He put me forward for the OVM- 200 phase 1 vaccine and is happy to discuss my plans ( sometimes with a raised eyebrow). He will want me to stay on current treatment till next year for sure.
Another year of ADT on top of the 18 months puts one at high risk for CRPC. Any treatment regimen, when continued without interruption selects for resistant sub populations. That is why I am an advocate of adaptive therapy, and I remain HSPC 15 years after diagnosis and 14 after BCR.
Consider the following small study of adaptive abiraterone compared to continuous. The article has a good introduction on why adaptive cycling is superior. Paul
You are probably aware of my adaptive Bicalutamide experiment so no need to repeat it here. By posting, I would like to comment on your proposed treatment:
1) Bicalutamide is regarded as the underdog when compared with the newer lutamides. All the latter being currently under patent with astronomically high price tags, is nothing but a "conspiracy theory". Yet, Bicalutamide is pure dynamite. My case is a proof of such an assertion.
2) Although our cases differ considerably in disease progression, my assesment is that you will not need such a MEGA dosage like 150 mg/day. Start with the usual 50 mg/day and if after 45 days, time to reach quasi-max serum concentration, your PSA isn't within your target count increase it to 100 mg/day and check again before resorting to 150 mg/day. But, I bet you, you will end up reducing the dosage, if like me you opted for a low PSA to the limits of detectability but NOT undetectable.
3) Final comment and most important!
Instead of intermittent semi-annually on/off switching find and maintain the effective dosage that will match and counteract any progression.
If in need of technical support going into this, I am here ready to assist. Scouts honour.
Brysonal - While I've had to interrupt my n=1 trial of bical +/- dutasteride (& now +/- tamoxifen), I would agree with Justfor_ re: bical dosage and it's effectiveness. My "interruption" is to get RT for progressing gynecomastia as result of previous ADT and more recently bical in 50mg or 25mg (half tab) dosages. I am getting setup and scheduled for the RT this week and have been on daily 10 mg tamoxifen for the last 2 months. The tamoxifen has worked fine, but the RT will get me off a drug that has has known side effects that I would rather avoid. I restarted 25mg bical due to rising PSA several weeks ago (to at least put a brake on the rise until the RT is done) - as I stopped it completely for Tamoxifen to get the boobie prize under control.
Justfor_ is the model for creating a personal dosing schedule. The standard dosages that come out of clinical trials are often the max with fewest/tolerable side effects and not adjusted at all for max effect based on individual variance (body size, differential metabolic rates, lifestyles, diets, comorbidities, etc., etc.). Justfor_ has expertly tweaked his dosage to arrive at one that provides an apparent steady disease state using no more pharma product than needed to do the job.
A fine example of the many patients here at FPC who are stepping outside the normal bounds of SOC to test other treatment strategies and generously sharing their results with us, Thanks to all who do that.
Most important, Best of Luck to you, Brysonal, as you continue to push the envelope with cutting edge treatments like OVM-200. A true pioneer in PCa immunotheraphy, may you find the perfect match for your next step in treatment.
Sometimes I wonder whether it is the Tamoxifen that does the job. I tried to halve the dosage to 5mg/day and within a week my sternum was etching strangely, regardless the ultra low Bicalutamide. Since then back to 10mg/day. So, please, check for any changes in your Bicalutamide effectivenes after stopping taking Tamoxifen. Hope we don't get a big surprise.
Justfor_ - my original plan was to get to <= 0.05 PSA with bical alone @ 50mg per day and add dutasteride 0.5 mg every other day and cut bical back to half tab daily with new labs after a month or so. I had just started taking the dutasteride (daily at first) about a week when I met with my RO.
When she wrote the tamoxifen script, she was adamant I need to stop bical until I got RT. I was due for a 10 year MO treatment review two months down the road, so I was somewhat unsure where that might lead. Turns out MO is fine with continuing with the bical +dutasteride combo. I decided to stop dutasteride about 3 weeks after I started it and was off all pharma except tamoxifen when I saw my MO. I had not planned to continue with tamoxifen beyond the 90 day script, but some have suggested that, as a pharma SERM, it might provide some extended benefit on a much reduced dosage? (say once a week.) Especially so, as my T continues to hang in the mid 600 -to-upper 700 range.
What I was getting to, in regard to your comment, is that my understanding is that, at least for women with BCa, tamoxifen is not supposed to overly interfere with bone health - as it acts on ER alpha and not ER beta? (I have not dug deep to verify this.) At my recent labs, my PSA had ramped up more than I expected and I had noted that Friedman had commented in his book notes that (via Bob Leibowitz clinical work) the combo of 5ARi and SERMs could cause a rapid rise in PSA (which would drop when the SERM was stopped). In the case cited by Friedman he was speaking of dietary SERMs, such as Flax, but as tamoxifen is a pharma SERM, I was on the lookout for a similar rise and immediately stopped the dutasteride and restarted the bical (half tab) when I saw it. Much speculation in the above and until I get back to some consistent routine, I'm just hoping my PCa is as confused as my dosing trial now is.
Hope all is well with you and very stable. Will share my results when I get back to a consistent dosing program. Thanks for your insights and comments, here and elsewhere. Paz - Ciao - K9
Thank you. cujoe and good luck with the radiotherapy. Another thing I am so thankful to Finland onco for. After confirming my ‘riddled’ diagnosis but agreeing to add Lu-177 immediately as I started ADT he picked up the phone to radiology on the floor below and within 10 mins I was having my breast buds irradiated before my first Degarelix treatment. This would not have happened in the UK as my RO is across town from my MO despite being on same MDT and the red tape to organise would not be one phone call and in!
It was a nothing treatment done in minutes and for which I am v grateful would recommend to anyone ( well anyone about to start ADT!)
Best of luck to you too and appreciate the support.
Along with full panel hormone labs and up-front DEXA & other critical benchmark scans, RT for gynecomastia should be offered (or al least discussed) before starting any form of ADT. In your case a sign of a good, caring doc. They often seem to be few and far between, but it seems you got to one at the right time and place.
Support is always readily available here. Stay S&W, K9
Agree with your sound perspective, Justfor. 50mg bicalutamide monotherapy is sufficient and effective option to ADT. Could perhaps be cycled to delay or avoid antagonist-agonist resistance emerging. Newer and stronger anti-androgens as monotherapy are also new possibilities to be explored. Darolutamide is particularly attractive due to lower SEs and less susceptible to resistance mutations.
Thank you. I did re read your posts tonight and noted your dosage research ( and also that I am not an engineer!). If I go this route I would gratefully accept your support. Not even sure if bicalutamide would be prescribed to me as a monotheraoy in the uk but will keep in touch if that’s ok.
The idea behind this is not confined to any specific drug. Can be implemented with anything as far as its effect can be controlled at will. The scope is to match supply to demand. For every cancerous cell that divides one should be killed or put to sleep so that the active population remains constant. The idea of "scorched earth" (read undetectable) is only good for warlords. It's not a surprise that hormonal treatment, as currently practiced, ends up with castration resistance. Napal bombs didn't win the Vietnam war!
If you decide I will be more than glad to assist, just ask. Thank You!
Really good point. Clearly ADT in its current form fails and there has to be a better way! Very very impressed with your hypothesis and logic and skill to action it! Thank you for the offer of assistance.
I have had it prescribed as a monotherapy but NHS would insist on the standard 150 mgs a day if my experience is anything to go by. To do specific tailoring of doses you might need to go off piste without telling them which could be difficult as you may need their support for other interventions in the future.
ah ok if the NHS will give it as a mono therapy then he will prescribe ( I am BUPA ) if he agrees it’s an option. Prior to the Finland opinion I was going to discuss staying on Apalutamide as a mono therapy following the trial that had Enzalutamide as a monothersoy arm that seems to have done as well as the ADT arm. Forgotten it’s name but follow the onco on Twitter and like his ‘outside the box’ thinking and challenge to the castration mindset.
As you say getting a non standard dose maybe problematic! Interested though ( but aware my history of disease progression to distant bone mets makes me high risk)
While following the discussion with great interest i am just wondering, as the final goal is to evade resistance, is not BAT is more clinical trial active (meaning more clinical trial are being performed and hence more doctors are involved) option than the intermittent ADT?
I'd seriously consider that but don't think we have a BAT clinical trial here in the UK. Whilst I've travelled for specific treatments I would have struggled to do the OVM-200 trial overseas and work full time. I'm not ready to retire despite turning 60 last month!
I will mention it to my MO but so far its been me introducing the clinical trial to him not the other way round!
Everything I had/ have done with Finland is 100% out of pocket private
My London RO/MO /Zoledex/Apalutamide is paid for by BUPA as part of my company private health insurance. He works in the NHS too but i wouldn't get the face to face attention without being private tbh.
The clinical trial for OVM-200 vaccine and scans therein is in the clinical trial unit of a London NHS Trust
My GP is NHS but I don't use them for much they just get informed of the plan.
unfortunately my G6 was not slow moving. I opted for HIFU originally as ‘on paper’ I was a perfect candidate but first one failed and my professor ( at top London focal hospital( said it was a tiny clean up job and did 2nd.
My PSA started to rise and a PSMA PET scan picked up a met at T1 and third rib. Shock all round. She said she had done 1,000 HIFUs and never had this happen. It’s nice to be ‘special’ but not this way. So G6 to metastatic in 3 months!
Maybe my soft choice whilst curable had led to my aggressive choices now I’m not!
Whatever u have done to get to mom- detectability IT HAS WORKED? But what contributed the most? Was it the vaccine OVM-200 or the Lu177 early use. Presumably the PSMA scan done after Lu177 lights up ZERO Mets in your entire skeleton?
Is there any data to show effectiveness of the OVM-200? What is your gut feeling on OVM-200 effectiveness for you. You got it for free, no side effects so great that u tried it… so now why not everyone try it?!
The only drug I have not mentioned is highT/ BAT but with non- detect ability no need to take this now , or do u have some PC cells that would be zapped in a high T environment but which are not seen at a micromet level. High
T can be a drug available in your back pocket?!
Again, I’m very impressed with the combos you have taken and keeping up the new technologies. Keep up the posting… and the undetectability!!
on paper it could simply be the hormone therapy doublet that worked and I may have had the same result at this point without the rest!
I did the triplet sort of with 3 Docetaxel rather than 6 with early Lu-177 for the other 3 infusions
So appreciate a SOC treatment could have left me in exactly this position
However post Docetaxel my scan is on my bio showed activity in prostate and T9 reduced by still with an SUV. So I did the VMAT which is again SOC and could have got me here but I also did 2 x Brachi and and SBRT to T9. Si added another radiotherapy triplet. Only went undetectable when Apalutamide was added so again SOC could have me in same position. No idea!
I could only get OVM-200 as I was completely stable and undetectable on bloods and scans. No idea if it’s triggered a. Immune response and hope it moves to a phase 1b now they know it’s safe
Only radiation kills the cancer, but you are right your PSA could be low on ADT+ Apalutamide.
I believe you did everything right except I would skip the double brachitherapy. Maybe I would SBRT my prostate, but maybe vmet is even better but I just wanted short.
My only regret is not contacting Finland as soon as I was diagnosed ogliometastic with mets to T1 and third rib. Whilst organising SBRT to these mets the only systemic therapy on offer was ADT. I'll never know the outcome of early Lu-177 x 3 plus 3 x Docetaxel on top of the MDT that I need get. I started them 10/11 months later than ideal but UK were not up on Lu-177 and wasted time speaking to the UK specialists who wouldn't help early/ Novartis who didn't have UK trials up and Germany who would take a booking but not offering a consult which was strange. Finland were the first time I felt I could have a complete convo about all including early Lu-177.
Heigh ho. I believe there is now a MDT plus v early Lu-177 clinical trial.
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