Got the results of the latest bloodwork today - my prognosis 0.1 measured 0.1 - put a smile on my face!!!
So things are proceeding in a steady enough decline that I can accurately predict the value 3 months ahead. (see the curve on my profile)
Take aways are:
no noticable different on the decline curve between using Xtandi at 120mg or 80mg.
The oncologist (a stand-in for my regular guy) wasnt too happy that I reduced to 80 from 120 - talked about the lower value resulting in a faster onset of drug failure - anyone got any ideas about this???
I also surmise from the curve that castrate resistance is not some magic threshold when all your cancer becomes castrate resistant, but that in addition to the castrate sensitive cancers some new castrate resistant tumours have appeared. The combination of ADT for the first, and Xtandi for the second is more powerful also for the castrate sensitive tumours as the rate of decline increases
The oncologist also noticed that my iron values were a shade low (Hemoglobin 11.4g/dl, EVF % 0.34) but they have been low since diagnosis. I didnt think that more iron was a good thing for PCa - I seem to remember some discussion of that on this site.
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Stoneartist
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I agree with your oncologist. I suspect you think PSA tells you a full picture of what is going on biologically- it doesn't. Remember that in trials of say, Zytiga+ADT vs ADT, both groups had the same initial PSA reaction. However, the group that also got the Zytiga lived longer and progressed more slowly. If you have a toxic reaction to the medication, cut back or choose a different one. If not, stick with the dose that was found to have the best therapeutic ratio in clinical studies.
Thats fine TA - but from what I read they only tested to find out what was the maximun dosage beyond which the side effects were serious. I havnt found anything which tested for the best therapeutic ratio in clinical studies. Do you know of any such studies. I see that it is normal for an MO to approve lower doses when patients show severe side effects, so they dont seem to be worried. Thats why I have tested by being on a lower dose between blood tests to see how it affects the PSA curve. The rate of PSA decline with Xtandi and ADT was a little faster than ADT alone which tests have established, but the rate of decline on 120mg and 80mg Xtandi looks to be the same. Xtandi reaches a saturation level in the blood which is quickly attained using the maximum dose of 160mg. It seems sensible that a lower dose is needed to maintain saturation. I am not planning to lower my present dose and I expect to be on Xtandi and Zoladex until something new happens - hopefully many years. Thanks for your input.
When you write:"I see that it is normal for an MO to approve lower doses when patients show severe side effects, so they don't seem to be worried." That is an unwarranted conclusion on your part. Of course there is a trade-off between lower dose and efficacy, but if a patient can't tolerate the most effective dose, that trade off must be made, unfortunately.
"I haven't found anything which tested for the best therapeutic ratio in clinical studies. Do you know of any such studies."There were many such studies. These, for example:
There were probably many more lab studies done by Astellas. They would have done the early pre-clinical studies that demonstrated the dose dependent relationship of the drug and its active metabolites on the AR. Do you imagine they just pulled the dose out of a hat? You also have to look at its active metabolites.
"That's why I have tested being on a lower dose between blood tests to see how it affects the PSA curve." As I said, that is a big mistake. You are attributing its biological effectiveness to PSA, when the true biological effect is on the AR. PSA is just a convenient rough biomarker.
" I am not planning to lower my present dose and I expect to be on Xtandi and Zoladex until something new happens - hopefully many years. " That is certainly your prerogative. But understand that you are demonstrating the Dunning-Kruger Effect, and you may be harming yourself in so doing.
Thanks for your input TA - I learn more every day. I need to digest the links you sent and may end up increasing the dose to 120mg - shall talk to my oncologist when he is back
I dont know - but I make a prediction from my PSA curve each time - and this last 3 months that prediction was spot on. I reason that when the newest result is significantly more than the prediction - then something new is happening.
A deviation from prediction could also mean that the biology has many more variables than the math is taking into account. Biology is very complicated, and I’d think it difficult to be modeled mathematically when we’re at the cellular and DNA level (e.g. PSA response).
But, I feel ya, brother. I’ve done the same type of thing. Sigh.
that you are smiling and feeling good about your treatment is a very good thing. I can’t comment on your treatment questions , your oncologist is the best for those …but I’m glad you are feeling upbeat for a change. That can be hard to come by hereabouts, good for you.
We all have that life which is served to us and we can not do better than squeeze every drop of good feelings out of each day. I recently stopped short while walking my dog and took a picture of a majestic old oak tree in the night, and was feeling that life is great at the sight.
Well I am doing just fine on 80mg so I dont plan to decrease to 40mg. Hoping the time to progression is measured in years. My greatest side effect is fatigue - and that I can tackle.
My main reason was twofold. First the phase 2 trials showed that the higher the dose the more damage (SE) Xtandi did. So the standard dose of 160 was designed to be the highest tolerated. But the active stuff in the drug reached a maximum concentration in the blood and I reasoned that we need less than this dose to maintain this saturation level - so the dose could be reduced to 120 - with less SE and the same Efficacy. Also there must logically be a difference between tackling a set of agressive tumours which are seen in a rapid rise in PSA - and tackling a near dormant set of tumours showing a PSA near nadir. I need to do some more study - especially of the articles Tall-Allen posted to follow this up. The other reason is that both my castrate sensitive and my castrate resistant tumour sets show a high PSA sensitivity - so while I can still measure the PSA decline on its steadfast path to undectability, I can alter the dose and see if it affects the decline curve.
I fully appreciate that the PSA is not the cancer, but in my case the PSA decline is difficult to explain with anything other than a further reduction in tumour activity so alterations in the decline curve may very well represent the efficacy of the drugs. I can only do this now because once my PSA in undetectable I have no markers to go on. The last 3 months on 80mg gave me a PSA exactly as expected from analysis of the decline curve - so it looked like 80mg was enough to zap any tumour growth that was beginning. I am thinking of going back to 120 for the next 3 months an looking to see if the curve is as predicted - ie no difference between efficacy in a dormant tumour environment between 80 and 120mg.
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MRI prior to HDR Brachy and HDR intensity.
PSA holding low!!
