On 5/12/20 began meds : Bicalutimide 150 mg, Finasteride 5 mg, Tamoxifen 10 mg
Background: April 2019 PSA 20 and dx w/ Gleason 3+4=7, July PSA 13, Nov. PSA 26 (and SCANS SHOW BONE METS), Feb. 2020 PSA 31. Still zero symptoms/pain.
I could not find an MO to do either high-dose estradiol (first choice) or commit to a BAT approach, so decided to start off with anti-androgen therapy rather than "standard" ADT (with an expectation of iADT in the future). Got the first lab results at a bit under five weeks:
6/15/20 labs
- PSA 6.4
- ALP 152
- T 1159
The bigger concern with these first labs was to make sure the liver was handling the meds, and yes, all the other blood markers seem to be in normal ranges. So, so far so good. NO side effects. While I am not disappointed with my PSA response, I don't really know what is typical for the number of weeks to expected PSA nadir. Any ideas?
Thanks to all those here (and elsewhere) helping through their posts and comments to inform my decision, like Magnus1964, Nalakrats, etc. Looking forward to continued support and conversation!
-Noah
Written by
noahware
To view profiles and participate in discussions please or .
Nadir PSA is defined as the lowest PSA obtained in first year of any type of ADT. (includes Bicalutamide)
The longevity depends on three factors:
(1) How low PSA reaches finally..lower the better.
(2) How many months it takes to reach at Nadir. Anything over 8 months but less than 12 months is considered a sign of long survival.
(3) An additional prognostic factor is Nadir T...here again it is lowest number of T which is reached in first 12 months of ADT. A total T of 10 or below is a great Nadir T.
If you reach PSA 0.2 or less...and take more than 8 months to reach there and you achieve
Total T of less than 10..you are very lucky and expect to live 10 plus years.
Thanks! The first two make great sense, but as for my T levels, I think they won't be dropping like a rock with bicalutamide only. Since it works on the AR receptor only, from what I understand the body reacts by still producing lots of T that can keep serum levels of both T and E2 pretty high (and thus the better side effect profile).
I think that's right. Bicalutamide may actually increase T levels but reduce uptake inside the prostate tumor cells. See: rxlist.com/casodex-drug.htm and search the page for "mechanism of action".
According to a study ...longer Time To Nadir has something to do with fibrocytes /fibroblasts activity. So, slower jorney to Nadir indicates true decline in cancer cell activity. A quick steep fall causing Nadir in 2 or 3 months can be due to androgen receptor transcription . I did not fully understand this theory so can not be totally clear about it.
As for over 12 months..it indicates slow very death of cancer cells ..so it may or may not be good.
Thanks! I realize that I am taking a "softer" approach. I did consider the aggressive multi-prong attack (as suggested by the likes of Dr. Bob) but have considered that my cancer MIGHT respond well to this approach. A poor or short initial response will be reason to re-think that, of course. But with 3+4 and a low burden of (asymptiomatic) mets, it hopefully is a marathon and not a sprint.
Maha Hussain found that men with a low burden of metastases responded better to continuous ADT vs intermittent with goserelin and bicalutamide. "The median survival after randomization among patients with minimal disease was 5.4 years in the intermittent-therapy group, as compared with 6.9 years in the continuous-therapy group " Since then, STAMPEDE has taught us that early use of Zytiga or Xtandi extend survival over Lupron alone.
To be clear, I will personally read that statement as "early use of Zytiga or Xtandi extends median STATISTICAL survival over Lupron alone." The thing is, we have different ways of weighing the info in these studies. I don't see any reason MY survival should be the median survival. Why would it be? If nearly ALL men survived a LOT longer, I would find the info a lot more compelling.
The only way I might be COMPLETELY confident that the stats conveyed an objective and universal reality that applied to me is if I looked at many differentiating facts about each participant in the study (and sub-grouped them accordingly), rather than regarding the participants as little more than a single homogeneous group ("men with minimal disease").
I also like to look at the survival curves (and how they diverge, and slope), not that I truly understand them. From this Hussain one, it looks like the statistical survival advantage is best for men who are going to live more than two years but die within seven years. For men living LONGER than seven years, it appears there was little or no survival advantage.
The iADT curve is concave-up while the cADT is basically flat. Then look at the curves for men with extensive disease, and you see the opposite: it appears iATD is initially MORE beneficial than cADT, but then at about eight years the iADT men start dying off much more quickly. And cADT men suddenly see a survival benefit?
If you can explain what factors or mechanisms might be behind these variations in concavity, I would love to hear some ideas. Over time, how does cADT go from being less beneficial to being more beneficial in one group of men, while doing the opposite in another group?
I try to consider what a "statistical survival advantage" of a year or so might mean to me. That I live for 3 years instead of 2, or 6 years instead of 5, or 14 years instead of 13, with standard cADT as opposed to iADT? That's not what I see in the curves. What I see is, the survival benefit (if any) appears highly dependent on how long I actually end up living!
At the five-year mark, 50 of 100 of iADT men will be dead but only 40 of 100 of cADT will be dead. My interpretation? Men whose cancers are not highly lethal are mostly ALL still alive. But IF you have aggressively lethal cancer, there's a very good chance you will be dead WITHIN about 5 years with iATD and dead WITHIN about 6 years with cATD.
Should I care? Well, I don't... unless you have a sure way of telling me I have aggressively lethal cancer, and will not be in that group of men living LONGER than seven years. (But not so lethal that I die within two years, because then I would also have no survival advantage w/ cADT, either.)
I am happier and less worried if I either 1) delude myself into supposing I will survive longer than seven years, or 2) tell myself that if I turn out NOT to be a long-term survivor, that's okay, too.
That is a little different than being completely fatalistic (why do ANYTHING?) but is more a decision to consider the marginal differences between known effective treatments to be just that: marginal. And I just prefer not to spend a lot of time worrying or suffering over things that may not make ANY difference, let alone even a small difference (especially if there remains a logical possibility the "softer" way proves to be beneficial rather than harmful FOR ME, despite statistical likelihoods).
That something makes difference statistically in the aggregate does not mean it definitely makes a difference in the individual, especially if you have the belief that a variety of factors not related to treatments are at play.
My core belief is that the predominant factor in longer survival is NOT the nature of the medical treatment, but the nature of the cancer itself and its overall compatibility with the human terrain in which it resides. Some men seem doomed to die sooner simply by the nature of their particular cancer/human ecosystem. That doesn't mean aggressive treatment is not helpful, but just that it may not be helpful enough for extended years of progression-free survival.
It's a philosophical difference in approach. I am more likely to see THIS as the takeaway from the study:
"Our findings were statistically inconclusive... too few events occurred to rule out significant inferiority of intermittent therapy. Intermittent therapy resulted in small improvements in quality of life."
Wonderful ! Brillient logical analysis. I think exactly the way you are thinking and I could not have said it better.
BTW, Maha Hussain;s study is contraversial as editors of journal concluded that results are "inconclusive" .
My bottomline is : Any treatment is good enough IF it brings your biomarkers in excellent level. Biomarkers are proxy for cancer cell activity in case of PCa.
If you drink river water and eat green grass as your treatment and your PSA becomes 0.2 and ALP less than 80...Hb over 13, LDH below 120.....from my point of view your treatment is working very well.
Proof is in the pudding....so numbers have to watched and effectiveness of treatment has to judged by these numbers. F..SOC...any treatment is good as long as it gives excellent results. Also, every one's PCa is different...ranging from indolent to super aggressive and anything in between.
You misinterpreted her wording because you and noahware don't understand research jargon. The study is not controversial. She, not the editors, called "inconclusive" the fact that they" cannot rule out a 20% greater risk of death with intermittent therapy than with continuous therapy, but too few events occurred to rule out significant inferiority of intermittent therapy."
Allow me to explain the jargon, which, I know is difficult for people like you who are unfamiliar with it:
• The study's hypothesis is that intermittent ADT (iADT) is not inferior to continuous ADT (cADT) in terms of risk of death. They are trying to reject that hypothesis.
• The researchers arbitrarily set a 20% difference as the "inferiority benchmark." They have to set a benchmark in order to calculate the sample size for the study.
• The study found that iADT compared to cADT was inferior by 10%. However, the 90% confidence interval included some men who were more than 20% worse off. In researchese:" The hypothesis that the hazard ratio for death would be less than 1.20 was not rejected because the upper limit of the 90% confidence interval (equivalent to a one-sided 0.05 test) was 1.23, extending beyond the noninferiority threshold of 1.20" On the other side of the distribution, the 90% confidence interval reached to 0.99, so "we cannot state that intermittent therapy was [statistically] significantly inferior to continuous therapy." This is what is "inconclusive" - they cannot reject their hypothesis, but neither can they confirm it statistically. Although, on average iADT was inferior.
So it's "inconclusive" that iADT was more than 20% inferior. But it was inferior by an average of 10%. Men on iADT survived 5.1 years vs 5.8 years for men on cADT. Husssain writes:
"However, given that nearly the entire confidence interval tends to favor continuous therapy, the result suggests that intermittent therapy may compromise survival."
In subgroup analysis, the difference in results were even more striking. Men with low metastatic burden survived 5.4 years in the intermittent-therapy group, as compared with 6.9 years in the continuous-therapy group.
Furthermore, they found no significant differences in long-term QOL. "Intermittent therapy was associated with improved erectile function and mental health at 3 months but not thereafter. "
So you have to think twice about advocating a therapy that may be harmful.
You are also completely mistaken that "My bottomline is : Any treatment is good enough IF it brings your biomarkers in excellent level. Biomarkers are proxy for cancer cell activity in case of PCa." The STAMPEDE trials proved the opposite is true - although ADT was able to bring PSA to undetectable levels, men lived longer when they added abiraterone, enzalutamide, apalutamide or docetaxel. We are lucky to have PSA as a biomarker, but it doesn't include micrometastatic cancer activity.
Also taking Bicalutamide ( but only 50 mg) , finasteride 1.25 mg and 10 mg of tamoxifen. Started 8/19 when PSA had reached 65 and tumor next to wall of rectum was inoperable. 10/19 - PSA 1.7. 12/19 - PSA .3. 3/20 - PSA .1. No side effects and continue walking 50 miles a week. Today’s round of golf will be 131 for this year. Bone scan and pelvic MRI 3/20 were clear. Quality of life was most important for me when deciding which hormone treatment to use. My oncologist recommended 150 mg of Bicalutamide but M O said to start with 50mg -so far it is working. Good luck.
You are a super responder and likely to live long. Walking 50 miles a week...nice...I am envious as I walk only 35 miles a week...need to walk more. But I do brisk walking with non stop music in my ears.
My MO suggested radiation instead, but my reading suggested tamoxifen works better. The MO felt there was not sufficient evidence to assure it was completely safe but he had no problem trying it out at 10 mg. For me, after a month, it appears to be working, and without any adverse effects. No breast pain, growth, etc. but also no apparent liver toxicity.
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
It's Back...
PSA lab results. How low do they go…
PSA time to nadir as a prognostic factor of first-line docetaxel treatment in CRPC
