Timing of ADT + Zytiga - Anyone else start them at different times?
I have locally advanced disease (+ pelvic nodes). My treatment is based on the intensification experiment in one of the arms of the STAMPEDE trial in which abiraterone (Zytiga) was added to radiation and regular ADT (i.e., Lupron) for 24 months in the experimental arm, with then Standard of Care of RT + ADT in the control arm. The benefits from the intensification with abiraterone in the trial were substantial in terms of BCR failure-free duration.
I started Orgovyx in July 22 but didn't start Zytiga until April 23. The reasons for the delayed start aren't relevant to my question. As I will have taken Orgovyx 24 months at the end of this June, the question that naturally arises is: (a) do I stop taking these two meds when each hits 24 months (this July for Orgovyx and May 2025 for Zytiga); (b) stop both this July; or (c ) take both until May 25?
I've gotten two different answers ( (a) and (c ) above) from two oncologists from two NCCN designated cancer centers. Ultimately it will be my decision to make, just wondering if anyone else is in this situation and if so, what guidance you've received. I'd like to stop both in July because I'm wearing down from the intensified treatment but don't want to compromise the results proven from the trial. Typical PCa dilemma!
Thanks!
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Edmond - that's interesting. By the widely accepted medical definition of cure, you were cured. At least 10 years with undetectable PSA. But only 2 months after that a BCR...wow. Thank you for answering my question. Only a 3 month difference in when you started Lupron and abiraterone, but the decision was that 21 months of abiraterone was good enough. Good to know!
Ok that clarifies their interpretation of psa.
Thank you,good luck on future tests I know this can be very stressful if u let it be. Always enjoy each day ,week,month,and year.
Indeed it is all interesting!
In the past year or so I did a blood test for genetics and it came back that I was likely to have BRCA2 mutation. With a family history (paternal grandmother died of ovarian cancer, material grandfather died of prostate cancer), my health teams feels that the BCR is "likely" because of the genetics. Figuring out how/why BCR occurs is definitely an area of interest that I plan to support.
In terms of my ADT treatment options, best to put the full discussion on the table for your consideration. After we found the cancer in 20+ lymph nodes, my doctor suggested triplet therapy (Leuprolide, Abiraterone, Docetaxel) but I was about to start a new job and didn't want to go all-in with treatment, especially the chemo (docetaxel). So, we stepped into this with a single treatment of Leuprolide and then 3 months later (PSA dropped from 19.0 to 0.4) we added Abiraterone and then 3 months later I was at "< 0.1". I've revisited the topic of chemo (docetaxel) and while my team would support if I wanted to go in this direction, their advice is to keep it in the tool kit and not use it now (and keep it available later, after it becomes resistant). So, my game plan is to finish up this 24/21 month treatment of ADT and then hopefully get off it. At age 53 this fall, my team feels that there is a "high probability of a modest recovery of my testosterone levels in 6-15 months".
I am keenly aware that every person has a different story, so my goal of sharing complete information is so that it either has matches to other people, or provides context of experiences.
keep the faith!
Absolutely and you are welcome.
The biggest change I made with my outlook on life is to shift from having a life expectancy of 90 to a life expectancy of 80. If I get to 80, that will mean I had won the battle of PCA for 39 years of my life, which would be terrific! In doing so, I've adjusted timelines and plan to retire when I'm in January 2028 (will be 56 and turning 57 that year), but retirement will just mean stepping out of full-time work and doing less. I work for the state doing 35 hours per week and work 2 days at home and 3 days in the office, so my job isn't too difficult as it is, but mentally (and financially) preparing for the off-ramp from full-time work is a big part of being at peace and enjoying each day.
I appreciate your elaborating on your treatment options. Only additional comment I'd make is that if you do indeed have the BRCA2 mutation then I'm surprised your care team has not suggested you look into PARP inhibitor therapy. I'm not that familiar with the SOC protocols for using a PARP inhibitor in conjunction with other SOC therapies, perhaps it is more of a last line of defense therapy.
I'm stunned that you've been dealing with this since your early 40s. Hats off to you and absolutely, 80 is a realistic goal if you have an oncology team that knows how to best employ the various therapies. I know an individual who has been battling Gleason 9 disease for almost 30 years. He was told by his urologist when first diagnosed back then to enjoy Christmas because it would be his last. He's probably outlived that urologist.
My Johns Hopkins MO just uses < 0.1 as undetectable. I get my labs drawn out of state (at Labcorp) and they don't use the ultra sensitive test. My Radiation Therapy was performed at Emory. Following my 37 pelvic radiation treatments they tested my PSA and they do use the ultra sensitive test and the result was undetectable, i.e. < 0.014. My JH MO believes there is too much fluctuation in the ultra sensitive test and he won't consider Imaging until my PSA is >0.1.
The only benefit from the ultra sensitive test,that I can see ,it will reveal a trend outside the margin of error.
you are welcome and yes.
Looking down the road, presuming the ADT remains effective for the 24 month period, I'll go off the medicine, but if the PSA rises, I’ll go back on ADT treatment. If at some point the PSA rises while on ADT, I'll add to the mix a combination of drugs of an Androgen Receptor Inhibitor (Enzalutamide) and PARP inhibitor (Olaparib). There is also a possibility that when/if my PSA rises after being on ADT, I might opt for an updated PSMA PET and if there are just a few locations, then radiation will come back into the conversation.
Onward to outlive my health team!
It seems that as of now, the scientific evidence is that at PSA less than 0.1, 99% of the cancer is dead. Some suspect that the 1% is also dead but there is no scientific proof as yet. They new hypersensitive tests can go down to PSA 0.003. Those labs would call that undetectable. It seems there are some scientists ware trying to show that PSA < 0.003 provides better outcome than < 0.1. It may be intitively sound. Proving it may take some years.
Dont mind me. I am just another layman trying to make sense of the whole thing,
It seems that as of now, the scientific evidence is that at PSA less than 0.1, 99% of the cancer is dead. Some suspect that the 1% is also dead but there is no scientific proof as yet. They new hypersensitive tests can go down to PSA 0.003. Those labs would call that undetectable. It seems there are some scientists ware trying to show that PSA < 0.003 provides better outcome than < 0.1. It may be intitively sound. Proving it may take some years.
Dont mind me. I am just another layman trying to make sense of the whole thing,