Hi,
Mikes PSA has been creeping along Xtandi since October 2018 going up about .5 from 1.0 to 3.7 ( 7/23) his ALP also had been creeping up from 100 in October to 162( 7/23) So they stopped Xtandi 3 weeks ago to prepare him for starting chemo. In those 3 weeks off Xtandi his PSA doubled to 7 and ALP increased to 221. Would this big increase imply that Xtandi had been working to a certain extent? Would going back on instead of moving to chemo be a good idea? Thoughts?
Xtandi was working. I had xtandi during chemo with taxotere. Had to stop after 9 cycles acct cumulative side effects were about to kill me.
Once you stop an ADT drug it gives the later cancer cells a chance to become resistant to that drug. There are other ADT drugs that you could try.
Magnus, I think there is some validity to intermittent use of ADT possibly prolonging the non-resistant, i.e., HS stage. We know that eventually PCa becomes resistant, at some point, for continuous users.
He can always rechallenge after chemo
Do you have any literature with stats on how often this re-sensitization happens?
Just very small clinical studies. Just try it - you have nothing to lose.
HUbby was on Zytiga for 7 months along with ACT 225. Although the mets have reduced dramatically except for a vertebrae and a small on left in pelvis, his PSA dropped after the first month and has triple since. Oncologist and Professor have both said not to stress out about the PSA due to reduction in bone mets. They have now stopped Zytiga and await to see what the next PSMA scan shows in September. If the two hotspots remain, they may suggest radiation. His bloods are otherwise all normal.
Sounds like the Xtandi was working. Pity you did not do some tests with Vit C via IV with the Xtandi, to see if you could extend the Xtandi run and avoid chemo - perhaps for years.
My doctor says that when the Xtandi quits working it will be chemo time again. Been on Xtandi now for 30 months and still working with eligard shots monthly
Agree with TA Dr. Sartor has told me he’s had some success using both chemo and BAT to rechallenge Xtandi once it fails.
I read I believe on on Onc Live that chemo kills those cells that have mutated and found a workaround to Xtandi allowing one to rechallenge with it. If I can find the article I’ll post it.
Ed
From what little I know, the slow but relentless rise in Psa while taking Xtandi or Zytiga usually means its stopped working, and Pca or the body has begun to stop these drugs working to suppress Pca growth.
I went to chemo after Zytiga stopped working after taking it for 8 months. I got the usual time for it to work. Some get more time, some less.
I then wanted Lu177 but doc said I should try chemo, and if that if did not work, and it probably would not, then try Lu177. So after 5 chemo shots Psa went from 12 to 50, so chemo sure failed. I waited a month. Psa went down to 25 and nobody knew why but PsMa scan showed more mets. I began Lu177 last Nov and had 4 shots, complete the 4 x 8week cycles in June, now Psa is 0.57, and good PsMa scan report. I am also on Xtandi ( enzalutamide. ) The chemo tends to make Pca respond again to Xtandi or Zytiga, seems like this is true, but no more new bone mets, soft tissue mets all not seen in scans, so docs are pleased with my response. Xtandi or Zytiga don't seem to kill many Pca cells, but are just extra strong hormone therapy where plain ADT fails, and during ADT suppression my mets all grew up big enough to be seen in scans.
It is probable my Pca will continue to grow and next steps would involve DNA analysis and maybe PARP but I hav eto wait until Psa goes back up. Scans show I have no mets that do not make Psma avidity.
Someone asked what PsMa avidity, or what AVID means. When they do PsMa Ga68 PET / CT scan, a small amount of harmless radioactive gallium is made into a watery solution, like saltwater, and mixed with a ligand chemical and this is pumped into a vein to circulate around and around the body in blood stream. The ligand chemical makes the Ga gather wherever Pca is located, because the Pca cells make what are PsMa receptors, and the ligand hooks onto these with Ga68. PsMa is Prostate Specific Membrane antigen.
We are all avid for food, and for love in our lives, we seek to eat and be loved, so avidity is just a plain English word for where something wants to attract something else. Anyway, where Ga 68 gathers at Pca sites and nowhere else due to action of ligand chemical and PsMa avidity, the radioactivity is then often strong enough to create a nice image of wherever the Pca is located, providing there's enough Ga68 that has gathered. Usually Psa has to be between 0.2 and 5 to get a good PsMa can image. The radiologists can tell by the color of the image on what the avidity is for Ga68, and the amount of avidity is called SUV, or Specific Uptake Value for the Ga68. The higher the SUV or the avidity, the more likely Lu177 or Ac225 will also be drawn to wherever Pca is located, but not much to anywhere else.
In Australia where I live, Lu177 and other "nuclides" like Ac225 have become available at Theranostics Australia since 2015 even though there is only phase 2 trial success, no phase 3 yet, So if ppl fail chemo, they can get anything they want, including Lu177, if its available. It costs usd $27,000 and the doctors are very nice and hospitals are best world class quality. I'm glad I got Lu177, and will get more if needed. A large range of cancer types can be treated by TA.
After Lu177 has done all it can do, there may be Pca that has mutated and has not attracted any Lu177, so it will be a threat in future so something else must be found. I think its better to get Lu177 as early as possible, then chase the other stuff after, not the other way around.
Patrick Turner.
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Slow increase in PSA while on xtandi 
