That's a difficult question to answer since castrate resistance is defined as progression after primary ADT only. Castrate means a testosterone level of less than 50. Zytiga goes beyond a castrate level of testosterone.
I think the more important question is: Does Zytiga taken before castrate resistance increase overall survival? That question was answered in the STAMPEDE and LATITUDE trials. Zytiga taken before castrate resistance does increase overall survival. That's the most important thing.
I was prescribed Zytiga after RP, IMRT, and Firmagon monthly. Dr. Scholz's group felt I could "cure" this . 3/14 lymph nodes removed tested positive and the UCLA Gallium PSMA PET scan showed several remaining node still intact were positive. 18 month ADT plus 1 year of Zytiga/prednisolone
Although I am in Dallas, I was in LA being treated by Dr. Mark Scholz's group (google his book on PC). They chose Firmagon for my initial shot since it unlike Lupron wouldn't cause a T surge. Since I tolerated it so well, I am staying with the monthly shot
It is true that the studies I referred to are only patients with bone mets, but as far as I know, Zytiga is only approved for metastatic prostate cancer.
Chris did not mention any bone mets, therefore I understand the doctor wants to add Zytiga because he thinks Chris is becoming castration resistant. I would not object doing that when you are castration resistant even if there are no bone mets. But I think Chris can avoid the side effects of adding Zytiga until the PSA value gets above 2.0 ng/ml.
I should have looked at his specifics. When he said Zytiga, I figured he was metastatic. When he said he was on the verge of CRPC, I figured his PSA was already over 2.
Ok, I agree you are becoming castrate resistant. Is your doctor willing to prescribe Zytiga? Technically, you are non-metastatic if your mets can't be seen with a bone scan or CT.
I went through a similar situation to yours. I had a fast doubling PSA, 3 weeks for me! I had been discussing it with my doctor for a while. But since I'd already had early chemo, he didn't want to start me before I became castrate resistant. He actually suggested waiting a little longer so we let my PSA go up. When my test came in at 26, he called me and said I should start Zytiga. He had it ready for my appointment and also scheduled the pharmacist for the same time to go over everything with me. My PSA quickly dropped below 1 and then undetectable soon after.
Doctor said I am becoming CR because the it took 5 months for my PSA to go undetectable. unlike previously. Also my T is not as high as it use to be yet the PSA is climbing rapidly.
My PSA as of yesterday was 3.5.
I restarted ADT yesterday Lupron and Cassodex.
really wondering if I should be on Zytiga and Lupron
"I restarted ADT yesterday Lupron and Cassodex. " As long as you are not on ADT, no need to discuss castration resistance. I have the impression you fight the PSA value but at the end of the day you have to fight the cancer. Do not worry if it does not become undectable, I will never get an undectectable PSA and still expect to live "forever". Just wait until the PSA value gets above 2 while taking Lupron and Casodex. Since you have lymph node mets, there are no trials that show that you will live longer if you start with Zytiga or Xtandi before that value.
The lymph node mets will increase the PSA value, but I have never heard that anybody died because of a lymph node met. The American cancer statistics show that patients with lymph node mets live just as long as patients without them. So try to relax.
If you do not like your lymph node mets you can get the pelvic area radiated or zap these mets with Cyberknife radiation. This will let your PSA value drop as well.
If you have a 5 week doubling time you should get a bone scan or an Axumin scan now. Better yet a PSMA PET/CT. This doubling time makes bone mets likely.
Hey Gregg, I'm G9,Stage 3 and no mets ( according to my 2 great Docs @ MSK). I've been on Zytiga and prednisone since March 1st. My dx was 1 ago, started with Casodex and Lupron.
I am curious to know what are the metrics that indicate becoming "on the border of becoming Castrate Resistant (per my oncologist)." Do you know what measurements are indicating that?
My oncologist said I am becoming CR as it took 5 months for the PSA to become undetectable (taking Lupron and Cassodex). Previous times, the PSA went to undetectable in a matter of a few weeks.
In STAMPEDE among metastatic men, the hazard ratio for failure-free survival was 0.31. That means that castration resistance was 69% less likely to occur if they took Zytiga + ADT than if they took ADT alone. In LATITUDE, the hazard ratio for PSA progression was similarly 0.30. Median PSA progression-free survival was 33 months if they took Zytiga + ADT vs 7 months if they took ADT alone.
My experience was that when ADT by itself fails with rapid increase in Psa, Casodex is added, and often Psa goes down a lot, but then that combination also fails after maybe 6 months, so Casodex is stopped, and Zytiga added to ADT, then the same thing happens, with Psa going down to maybe 2 from 7, then this fails after say 8 months, and that usually signals the end of being able to keep Psa low with chemicals. But while Psa is kept low the mets can all grow and then you need to start chemo. This didn't work for me and Psa went from 12 to 46 after 5 chemo shots, so I waited a month and Psa went to 25 for no known reason but bone mets increased. Then I began Lu177, and after 4 shots with Xtandi added after No 3 shot, Psa went to 1.6. Its not a spectacular Psa reduction, but the last PsaMa scan shows huge reduction of mets all over and Psa has steadily reduced and is now 0.4.
If I didn't have Lu177, I'd maybe be having palliative care now, ie, waiting to die, needing pain killers. But I am back on my bicycle again. I have no idea how long this reprieve will last. But all this stuff happened between diagnosis that was too late for RP with Gleason 9 inoperable, because of my low Psa in 2009 up to now. The chemo is said to make drugs like Zytiga and Xtandi begin to work again, and for a longer time.
Pca as been constant threat for nearly 10 years. I should have been diagnosed at Psa 3, in about 2004, and maybe an RP would have been successful. Then I would not be posting here, and the cost of a long fight would not have been paid and I would not have endured accelerated aging due to all the treatments combined.
Shoulda coulda. An Americanism. You know the recurrence rate from rp is significant. The surgeons don’t brag about that. You are a fighter and have done well. Getting colder down under? Take care
Success of RP can largely depend on the skill of the surgeon to get every bit of tissue out that has any prostate DNA within it. This is not always the case, and any prostate tissue left behind might develop Pca in time, like the cells in the initial tumour at PG. The distance between cancer site and operation site is less than 3/4 " or 20mm, so chance of some Pca remaining behind is high.
One man I knew was so worried by spread after surgery that he had his PG and his bladder removed, and had ureters joined to a stoma inside of lower abdomen to fit a plastic bag for urine. The prostatic ureter was cut off and penile ureter sealed off low as possible. He had immediate total permanent ED. But then he never told me if he found that Viagra worked. He did not have the problem of waking up 4 times a night and could go much longer between pees in the day, like a 25yo, and he didn't need ADT, and retained full testosterone levels. Without testosterone, the penile function is totally ruined, because the erectile tissues fill with fibroids and there is zero pleasure or ability for any happy ending.
About 50,000 ppl in Australia wear a bag for pee, and some have another for solids. The operation of bag install is much more expensive than RP, but if you have the money, there are urologists who do it. There are a whole range of ppl with bowel and bladder problems needing a bag fix, plus a few soldiers or car accident victims who suffered massive injuries.
Now this man has never had to worry about Pca any more, but then he was also so lucky because he had this op before any Pca spread occurred, and this was way back in about 2011, and there were no scans sensitive enough to prove he had no Pca spread. Well, its a bit the same now, even the PsMa scan cannot see microscopic mets.
And from little things, big things grow.
When one sister of mine got a small lump in a breast that was positive, she had a double mastectomy, at 64. Then she had chemo and ADT, and is still alive OK at 75. Unlike before she turned 64, she now has zero desire for any relationship with a man. But has a lot of friends, always out and about, independent. She dodged the Long Fight that is so common for many women.
My other sister got ovarian cancer and she died within 18 months, big op, 4 chemo shots, lots of mets, nothing stopped it.
I’d like to know the answer to that too. We were told that taking it before we were castrate resistant would improve the length of time my husband had left, but I didn’t think to ask why this was the case.
Chris. Good morning. My dad was almost castrate resistance last year, his doctor put him on zytiga and his PSA has been decreasing since then. We went this way because at 87 dad was not a candidate for anything else. Hope this helps. Fight the monster 🙏🙏
It helped my Dad, his PSA was going up even as he was taking lupron shots. He started taking zytiga and his PSA has been decreasing since, 87 and been on it a year.
Interesting reading. I’m one of the 1900 men in the U.K. who were asked to join the Stampede trial, taking Zytiga, Prednisone and Zoladex from diagnosis. PSA at dx was 571, multiple major bone Mets. Zytiga cuts another pathway from the adrenal gland for PCa to feed and mutate. Results 4 years ago showed a 40% increase in OS. I’m currently at nearly 8 years, last PSA was immeasurable. Sounds good to me. No dietary changes, no supplements. Maybe I’m a super responder, but I’ll take that.
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