Something to keep in mind. This is from a Danmeade interview:
TRANSFORMER
“However, the real difference between the treatment arms was seen after cross-over – when men on BAT were switched to enzalutamide or vice versa. “If we gave BAT first and then enzalutamide, almost 80 percent responded, and the response lasted almost a year. That’s quite an improvement in the rate of response and duration.” Among patients who received enzalutamide first, followed by BAT, the response rate to enzalutamide was only 23 percent.”
Keep in mind: everyone in the TRANSFORMER trial tried and failed Zytiga first. Normally, Xtandi is of limited value after Zytiga. So what BAT seemed to do is restore sensitivity to Xtandi. In the RESTORE trial, BAT was able to restore responsiveness to Xtandi but much less to Zytiga. The reason for the difference is not understood. Unfortunately, although BAT restored sensitivity to Xtandi, there was no significant increase in survival. The vacation from side effects is worthwhile.
For most, I'd assume. In the RESTORE trial, there was no benefit to rechallenge with either Zytiga or Xtandi in men with the AR-V7 mutation. AR-V7 prevents much benefit from Zytiga or Xtandi. So, I'd assume that most of the Zytiga men had some benefit before it failed.
Just want to comment as my husband is one of the few men on this forum who did BAT with the TRANSFORMER protocol. He got about a year from Zytiga before it failed, then switched to Xtandi and got another year before failure. At that point chemo was SOC but he chose BAT instead as he had doctors who were willing to prescribe T. After Xtandi, he had 10 successful months of BAT when psa dropped dramatically. He is now back on Xtandi where his psa has dropped again but he has a lot of unpleasant/debilitating side effects. So my point is not to get too caught up thinking if you've already had Xtandi that BAT won't work. Finally, TA can you cite your source about survival rate? You quote it a lot and our oncologist disagrees, so want to read the source.
This review states "OS in men receiving BAT→E was 37.3 mo, exceeding historical expectations"
It might take a while to gather all the info (dates, etc) but I'll work on it.
in reply to
I'm not sure about what Scout would like to see, but I'd be interested in Gleason score, grading, and what procedures were done. With approx dates. A PSA history but just approximate would be more than enough.
For me:
In 2015 my PSA rose above 4 and then went continued to 12 in 2018. I ignored my PCP's advice to have a biopsy when it went above 4 (I was going to Cabo and happy to have a STUPID excuse). Finally in 2018 I had a biopsy and was graded 3+4, T1, local and minor.
I had RP later in 2018. Regraded 4+5, T3b/c, N1M0. Bad stuff. The first PSA test post-surgery was 3 weeks later and my PSA was zero.
4/2019-9/2018 estrogen ADT therapy with Zytiga (still on Zytiga today but stop it for a bit and then restart). PSA held around zero. Testosterone<4.
9/2019 casodex 150 mg/day and dutasteride 0.5 mg/day. PSA zero.
9/2019 - 8/2021 high testosterone (cypionate 400 mg per week). PSA zero and slowly rose to 0.17
9/2020 MRI and CT scans clean. MO talked me out of radiation.
8/2021 Started BAT. PSA went to 0.2 on high phase. Zero on low phase. I'm on the 7th month. Last cycle PSA went to zero on the low phase.
I'm going to discuss the next step with my MO. BAT won't last forever (unless it does :). I optimistically guessed 6 months. Not sure if I can do Xtandi or Zytiga or RT and then BAT again. No trial that I know of for HSPC.
That would be nice! If that happens I might not need any other therapies.
I'm undecided about the length of the high phase. Some research points to longer cycles, some to shorter. It would be nice if a trial was run with varying time frames. I can test to kind of figure out low durations and let them be PSA-driven. I can't do that with high cycles. Maybe some kind of proxy?
I have two theories:1. Two major cell tribes. Androgen sensitive (ASC) and androgen insensitive (AIC). On the high phase of BAT ASC goes to town, it's a testosterone smorgasbord. AIC is weeded out. Switch to low. AIC likes it but ASC (the bulk of the cells) are starved. Cancer grows but slowly as you weed one population and then the other. But never completely destroy one to create the organism vacuum. For #1 to work there must be smaller tribes. Perhaps AIIC and ASSC and AISC and PRLC...
2. As the low T phase goes on, ARs are upregulated and mutated so that the cells can live with very little testosterone. Now you swamp 'em with tons of androgens. Bummer for them. Overload. Perhaps also DSBs or Ca ion influx. Now they figure out how to live in a high testosterone environment and boom! T is dropped. ADT phase.
Just like many sports. Get 'em used to one thing and they start to adapt to it, then boom! change gears and deliver the knockout.
#2 seems more likely.
End result though is almost the same thing.
But I keep wondering about the timing for killing off AIC and ASC or allowing mutations/upregulations. I think that much of the rest can be figured out with testing, clinical trials, and theories. I started at two weeks for hi T but have gone up to 1 month - unfortunately, the change wasn't as data-driven as I would have liked. Do you know how Patrick chose to go from 1 month -> 2 -> 3? PSA values on the high cycles or PSA values on the low cycles?
I watched Liebowitz's videos in 2019. I went to compassionate oncology a couple of times. Liebowitz was in the process of retiring and in many ways the remaining guys seemed more SOC than my SOC MO!
I'll message him. But what can I learn from a noob with only 17 years under his belt
As do I from his messages and posts. I wish I was involved in those lunches!
Consider: That the cycling of T is addressing population dynamics, just as you have summarized. So the rate of reproduction and growth of the cancer should relate and give some guidance in selecting the timing of cycles. For me, with very slow growing cancer, I choose longer cycles (2-3 months highT, 1-2 months low). For someone with short PSADT it would make more sense in theory to use shorter cycling. It just a theory to consider.
Makes sense. Normal prostatic glandular cells live around 500 days.For PSADT calcuations do you use the high PSA for each cycle? (Mine goes to 0.2 on the high cycle and zero on the low - this cycle the highest I measured was 0.3)
Visited Scott in Prescott last year. Didn’t know you were in Phoenix or would have come to visit and meet you, Russ.. Maybe in the coming year. We love to travel to the Southwest in the spring from Oregon, with wife in RV and me on motorcycle. We are “of a feather”.
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BAT: transformer trial
Exploring options: BAT, Docetaxel (again) ARV 110
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