I just finished 3 years of treatment with Xtandi (enzalutamide) with my psa going from 6.80 (07/19/17) and dropping to a low of 0.23 (03/15/18) . My psa then began a steady climb to 3.19 (08/02/19) and continued to 9.32 (07/16/20.
Prior to the Xtandi treatment my line of defense included the following: 06/2014 Elligard and Xgeva, following a determination that scans showed numerous metastatic deposits, APC determined. 06/2017 started Provenge treatment.
.My profile showed all of this started with RP in 06/2006 and EBR in 02/2008. Sorry to drag on but thought I should recap a few things.
I started Zytiga (Abiraterone) 28 days ago and just received my first lab...PSA jumped to 14.16. That put a scare in me. Can anyone relate to this large jump or does that say that Zytiga is not going to work for me and that I’d better get on to another treatment?
Thank you for your time!
Written by
docbulldog
To view profiles and participate in discussions please or .
Zytiga is unlikely to work or unlikely to work for long after Xtandi. It's best to alternate anti-androgens with chemotherapy , the results are much better (see the recent CARD trial).
The median rPFS with cabazitaxel was 8.0 months versus 3.7 months with abiraterone or enzalutamide, which translated into an overall decreased risk of progression of 46% compared with abiraterone or enzalutamide.
Hi Gregg, so to get this right in my mind, are you saying that once you become resistant to a line of hormonal treatment, go for the chemotherapy route then once this has had it use, go back to a other hormonal therapy again? Thanks in advance
Yes, that seems to have the best results because there is cross-resistance between second-line ADT agents. That was what they showed in the CARD trial with Cabazitaxel VS the other second-line when either Xtandi or Zytiga was first used. You are better off coming back to the other second-line after chemo, you might regain some sensitivity at that point.
I appreciate your response, my treatments started back before chemo was the first line that people are receiving now. I’m sure I’ll be working that direction even though my doctors are hoping to try other means first. Thank you
Good question, seems like they want chemo as kind of a last resort, we’re hoping something else comes along that is better, possibly a trial of some type. It definitely is part of discussion tomorrow. Thank you.
Really bad idea to use it as a "last resort." It adds 1 ½ years to survival when used early and only 3 months when used late. Also, side effects are MUCH easier when used early. Maybe find a new oncologist who knows this stuff?
Hi Allen, my father has just recently been placed on Enzalutamide alongside zoladex. Do you think he would be better off having chemotherapy alongside the zoladex initially as opposed to Enzalutamide or does it make little difference either way? Many thanks
I don't think there is much of a difference. I would argue for Chemo first on purely logistical grounds. He will be finished with 6 infusions in 15 weeks. After that, he can use an advanced hormonal therapy, which may last 3 years. If he does it the other way around, it can be over 3 years before he gets to try docetaxel. Also side effects of docetaxel are milder the earlier it's used.
Question for you TA: I'm on Eligard and added Erleada. If a fellow is still hormone sensitive and added docetaxel at this point would the year and a half survival kicker still apply? That's my game plan. I'm just waiting to see if I hit undetectable this week before considering adding the chemo. Thanks!
It was 1 ½ years if newly diagnosed, 3 months when used towards the end. I'd guess that somewhere in between is somewhere in between - but I'm guessing.
Looking at the ENZAMET trial nejm.org/doi/pdf/10.1056/NE... (p 130) it looks like the early docetaxel therapy really didn't have any real benefit over straight up enzalutamide. Am I interpreting that correctly? If so, apalutamide may be the same. That's what I'm looking at right now. Are the side effects worth it unless pain is involved in the later stages of the game? Decisions, decisions. Thanks for your input. Much appreciated!
I don't think you are interpreting that correctly. In ENZAMET, both groups had high (2/3 - 3/4) use of docetaxel. The trial was not designed to compare enzalutamide and docetaxel.
There was a STAMPEDE trial that compared docetaxel and abiraterone. It found: "This direct, randomised comparative analysis of two new treatment standards for hormone-naïve prostate cancer showed no evidence of a difference in overall or prostate cancer-specific survival, nor in other important outcomes such as symptomatic skeletal events. Worst toxicity grade over entire time on trial was similar but comprised different toxicities in line with the known properties of the drugs"
Give it another month. You may be experiencing the PSA bounce. When cancer cells die they give off PSA. So if a lot are dying from the treatment you get a ride in PSA. If this is the case your PSA should drop next test.
Both Enza & Abi, while quite different in their approach, target the androgen receptor [AR]. There are various ways in which the cancer might become resistant to one or the other, but, unfortunately, there is great overlap. So it is common for patients to see no benefit after switching. Example, if you became resistant to Enza due the emergence of AR splice variant AR-V7, you would also be resistant to Abi.
If you are resistant to Abi, you need a therapy that does not target the AR axis.
Alternatively, you can try to restore sensitivity to Abi/Enza. For example via BAT [1]:
"400mg intramuscularly every 28 days" i.e. of testosterone cypionate.
"Results: 5/29 (17.2%) of post-abi pts compared to 9/30 (30%) in the post enza group achieved a PSA50 response (P = 0.36). Post BAT rechallenge with abi (n = 19) or enza (n = 22) resulted in a PSA50 response rate of 15.8% (n = 3) and 68.2% (n = 15), respectively (P = 0.001). The total duration of benefit (i.e. PFS on BAT + PFS on rechallenge = “PFS2”) was significantly longer in the post enza vs. post-abi patients (Median PFS2: 12.75 vs. 8.125 months; P = 0.04. Lastly, AR-V7 negative (n = 42) pts has a significantly longer median PFS2 compared to AR-V7 positive (n = 10) pts. (10.3 vs. 7.1 months, P = 0.005). Conclusions: Our data suggest that BAT may be more effective at resensitizing mCRPC to direct AR antagonists (i.e. enza) compared to abi. Detection of AR-V7 portended a worse outcome on BAT/rechallenge."
Here in Australia, if you have ADT failure with Lupron, Lucrin etc, maybe after several years of suppressing Psa rise by reducing Testosterone to low levels, Cosadex is added to ADT to give some additional time to stop Psa rise and keep Pca growth slowed down.
But then we so often find after maybe 6 months that Psa rises again and so the Cosadex is stopped, and most common next hormone manipulator added to ADT is Zytiga. In my case Cosadex worked for 6 months and Zytiga for 8 months, and I ws not allowed to switch over to Xtandi because its well known that this change will not work very well and under our Australian Medicare rules its illegal for doctors to switch from Zytiga to Xtandi, or from Xtandi to Zytiga, and when both have been used at same time, it was found to have a disastrous outcome, so that is also banned.
Next normal protocol used to treat Pca after failure of ADT + Zytiga OR ADT + Xtandi is to have chemo. But I was told by my wise oncologist that chemo was unlikely to work at all, and it didn't, because Psa went from 12 before to 50 after 5 chemo shots, so chemo was declared a failure. But my good oncologist was happy to refer me to doctors giving Lu177, which worked a heck of a lot better than any chemo could and with far less side effects.
But mean time for successful killing of Pca cells to reduce Psa is 14 months, and that's about what I got. A research doc said I should have Xtandi added to Lu177 because it raised PsMa expression thus making the 4th Lu177 more effective in May 2019. Psa went from 25 at before Lu177 began in November 2018 to a lowest figure of 0.32 at 12 months later. Then Psa worked up again to 30, and last July 2020 I began a second series of Lu177 shots to attack survivor Pca cells in my bones. Psa has halved since 24 July 2020 with one shot of Lu177, while continuing with Xtandi and also taking Veyonda ( Idronosil )
A halving of Psa in one month is so far a much better outcome than outcome in January 2019 and March 2019 when Psa went from 25 to 17 only over about 4 months.
The added Zytiga after 3rd shot of Lu177 in 2019 may have made 4th shot of Lu177 more effective, and lowered Psa, but I think Xtandi stopped having Psa lowering effect maybe in December 2019, but its supposed to keep PsMa expression high even without lowering Psa and rate of growth of new + old mets, so I am continuing to take Xtandi, allowed under the Medicare rules and funded, and although chemo didn't work, it is thought it re-sensitized my Pca to get a Psa suppression for maybe 12 months, maybe aiding the Pca killing effect by Lu177, which goes on for quite some time after having Lu177, because radiated Pca cells might keep living for awhile, but when time comes for them to divide and grow, DNA is so damaged the growth fails.
Docs expect this second round of Lu177 to work quite well again, and in another year I may need more Lu177.
I had a friend who had RP, and Psa went low, but bounced up in 3 months, and same for ADT. Cosadex increased Psa from 7 to 40, and 10 shots of Docetaxel caused initial lowering of Psa from 40 to 2 for a few cycles but was back up to 40 after 10 shots, and PARP inhibitors were used but Psa went fast to 432, and mutated forms of Pca sprang up like mushrooms, and he got so sick with a liver riddled with untreatable mets that Lu177 would not have worked, and he soon died. He may have done better if he'd quit chemo as soon as Psa went up at about 4 shots, and had Lu177 asap, but nobody really could have predicted how he would fare if that happened. He lived only 3 years after diagnosis and his Pca outwitted all the best doctors. So when a drug makes Psa rise, beware, and be prepared to quit that drug and try something else. Its no good betting on a slow horse.
My Pca probably began in 2004, and before Psa reached 3, and by time it reached 5 action was taken to diagnose in 2009, and Gleason 9 inoperable was found when I was 62.
I am still alive at 73, and yesterday I cycled 84km at good speed, and felt very well.
Hi Bibsie, when I had main EBRT treatment back in 2010, I cycled 17km across town to get it for first 2 weeks but then I got too sore in plumbing below that I quit the bike and drove over for next 3 weeks. Usually there were 10 other ppl there waiting for their turn to have beam radiation, and I'd be all chirpy and say hello, but most were completely unresponsive, and didn't want to talk to anyone else, so it was jolly as a morgue, but I guess many knew they were gonna die, or just deeply depressed and distressed by needing to be radiated. The happiest person there was a man about my age who worked at a palliative care place and he got Pca like me. When I appeared in lycra, to most others I seemed like some incomprehensible cheerful alien who seemed out of place. EBRT was to me just another hill I had to ride over.
I had burning sensation when I peed after 2 weeks, and it lasted 3 more weeks of RT and about a week after, then eased down, so then I got back on bike asap like nothing had happened and all was OK. But during month off bike I swam a bit, only 250M a day, but better than nothing while I took it easy.
Bowel upsets and bleeding occurred later, but I kept cycling through all that time and only once had to stop on a ride to pee, and I could not control pooing, so I had to look for some amoung bushes to let it out, and then have a good clean up at home.
The bleeding became very infrequent and stopped, ADT continued, and I worked OK and cycled OK and Psa stayed low, so life went on OK.
I had a ureter between L kidney and bladder which became constricted during that time which needed 18 months of having 3 temporary uretic pig-tail stents inserted, and these made me bleed after insertion until enough temporary scar tissue formed and my body got used to them. I was able to cycle 90km with those stents. When a permanent stent was inserted, It didn't stay put, and about a month after insertion I peed it out, and took it to a doctor who said "That should not happen" , then I commented "Yes doctor, but shit happens, OK" and we both chuckled, and he sent me to hospital for 2 days of observations and a scan that showed ureter was working OK again and I have not needed any stent since. But I could have lost a kidney. I think my cycling fixed that problem like it fixed other things. Nobody knew why a ureter would stop working, but it did, and it wasn't anything to do with Pca or EBRT because it was diagnosed before I had diagnosis of Pca in Dec 2009. I'd hit a piece of wood on the road and the bump to me and bike shook up my internals so much it dislodged calcium build up in ureter and pee went cloudy for awhile, because the BANG shook out a bit of calcium. So I was diagnosed for ureter bother before I may have had one kidney fail.
I didn't fall off the bike when I hit the bit of wood, but I bent a front wheel and the frame a bit. I moved to bike No 2. I got bike No 1 fixed.
Interesting post Patrick I’ve never been unhappy doing palliative radiation, SBRT OR Abiraterone., and joke with the staff. But then I’m only 58 not in my 70’s or 80’s so I just continue my soccer , golf , swimming biking and hiking albeit at a slower speed as the years go by.
I know it's too late now for Docbulldog, but this information could help others. According to this study men having Abiraterone first then Enzalutamide second had better outcomes.
Few people3 seem to agree or care about this but it's my personal opinion that a diet high in lycopenes can cut back on growth of cancer cells throughout the body, when you do it right. You have to consume every six hours a quarter cup of V8 or tomato juice, low sodium to prevent high blood pressure. It causes more t-cells to get into the blood and is supposedly effective in causing apoptosis and slower growth of prostate cancer cells. Its cheap and easy but the main question is "can you stand it"?
Another thing, if you are able to look outside of the drug question, is heat. All cancer cells die at 106 degrees F. If you know the exact location of a tumor you can apply some heat to it with various means. I have been doing this for a couple of years and it seems to cut back on the growth but I cannot say it eliminates the pc totally. Similar for portable sauna.
Still one more thing is negative (south) magnetic fields. I've been trying this for many months lately and it seems to act similar to heat. It cuts down on the growth but does not eliminate the tumors completely. It eliminates or reduces pain due to tumors in lymph nodes in my back.
Lately I had a shot of Lupron (with Xtandi every day since), and my PSA has fallen from 35 to 0.8 and next check I hope will be near 0.1. That is over eight years since my discovery of stage 4.
Just wanted to put in my 2-cents. Why no Lupron? Isn't it standard where you live?
106F is 41C and its almost impossible to get the body temperature up above 41C, even if you hop into a hot bath of water, and run more hot water in to increase the temperature.
I doubt bathing in hot water kills Pca.
Eating huge amounts of tomato juice also probably has zero effect, and no trial has ever established its useful therapy.
But when you say south magnetic fields help, then you have me smiling, because that's like saying being close to a big electro magnet's southern pole, you get a fix for cancer, but not when exposed to a north pole. But magnetic field lines of force are assumed to travel North to South, and thus if you are at a north pole of a magnet and have lines of force travelling through you from N to S, all you have to do is turnaround 180 degrees and lines of force travel in opposite direction. I cannot see how magnetism in any shape of form stops Pca one bit.
If you have an electric blanket connected to mains 50Hz or 60Hz frequency, then you have a low level magnetic field that changes direction at same frequency. Some ppl say they are very allergic to all forms of changing magnetic fields in any electric appliance and allergic to all forms of electro-magnetic radiation from radio, TV sets, mobile phones et all.
I think they allergy is just irrational behavior, but they really cannot do anything about the amount of magnetic fields and radio waves and cosmic rays et all constantly flowing through our bodies all the time.
But go back to south magnetic pole. What magnetic field strength do you suggest is best? If you make a nice large electro magnet with thousands of copper wire turns around an iron core, and apply enough Vdc to make Idc high enough, you might get maybe 1.6 Tesla field strength between the poles of the magnet, and I ask, "Is that enough to make Pca die soon?"
I know more about electro-magnetic behaviour than most ppl, as my website explains at turneraudio.com.au.
I have found electric blankets turned up too high make aches in back worse because the aches are from getting old and getting arthritis, and I prefer a not-too-hot bed at night. I've heard ppl say I ought to sleep on a magnetic blanket which has many small permanent magnets sewn together and placed on top of a mattress, with a thick blanket cover to make it all comfy. To me its all irrational, until proven otherwise.
I also think you are lucky to have such non aggressive Pca. But getting Psa from 35 to 0.1 with Lupron + Xtandi does not mean your total amount of cancer cells has reduced by factor of 1/350. It just may mean the Lupron plus Xtandi has slowed down Pca activity that much, put your Pca to sleep for awhile, and when asleep its still alive and subtle change occurs to DNA to make it resist the effect of the ADT + Xtandi, and so your Pca may well begin to wake up, grow faster, and make Psa rise and ADT + Xtandi will seem to be useless.
I went through this with 6 years of Eligard, then Lucrin, then Cosadex added, then Zytiga added, and then chemo didn't work. I then needed Lu177 to kill Pca better than anything else, and I really do doubt that tomatoes or magnetic fields could have done anything.
I also tried high strength cannabis oil ( Sativa grown by a friend ) and bitter almond kernels with high amygdalin content, and Psa change just didn't happen at all. Baking soda is also another useless remedy imho, and also Essiac tea. These may all have placebo effects only, but reality is that the Pca slowly works to grow. It rarely goes into remission spontaneously.
Pca may not kill us; we may die with Pca and die from something else, but Pca is often a chronic disease as it has been for me since it began in about 2004, but diagnosed in 2009. I just gotta live with it, and if I followed any advice to only get alternative remedies I'd have died years ago; I prefer doctors. But I eat about 4 tomatoes a day in a salad I have 365 days a year, because I enjoy the taste and general effect salads bring, its all so much better than the junk food which food industry begs us to consume, to make us sick, and make profits doing that.
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.
Zytiga vs. Xtandi vs. Radium 223 vs. Cannabis
Latest PSAs BEFORE & AFTER starting Fenben/Hookworm Med. ~~so far so NOT good. Still optimistic for a reprieve, but PSA is heading UP UP UP
What Follows Lupron and Zytiga?
Zytiga failed, starting Xtandi. What to expect for my dad. 
ADT Vacation over?
