What is the relevance of this term and how does one know if it applies to them? I am stage 4, three mets in the back for which I have already received radiation treatment along with same on prostate. I have had 2 Eligard shots and been on 500 mgs of Abiraterone plus 5mgs of prednisone daily. Can I assume I am Castration resistant?
"Castration resistant": What is the... - Advanced Prostate...
"Castration resistant"
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GrantB47
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It means PSA is rising or metastases are increasing in spite of ADT or orchiectomy.
So, would it be too simplistic to simply say that castration resistant means that the patient seems to be losing the battle with the current treatment?
It means exactly what I said, not what you imagine.
Please, if I should happen to ask another question, don't answer it.
If you don't like my response, ignore it.
Others may find the answer helpful even if you don't like it. Best way for you to get an answer relevant to you is ask your Oncologist. Making assumptions might result in you pushing for bad treatment for you. Ask questions but accept anyone answering is trying their best to answer honestly from experience with this frightening diagnosis.
Uncalled for. Tall_Allen is one of our most expert members and was trying to help.
He just needs to work on his bedside manners.
Sounds to me like he was being a prick.
He is clinical, accurate, linear, and only uses facts. I find him extremely useful. He is removing assumptions not supported by fact.
The horror to know there are MO, RO, etc 'professionals' that treat you with this same exact prepotent attitude. At least this forum is free. It gets worse when you get billed for it. 😑
Thanks T A!
what do you mean by " losing the battle" ? How long since you have been diagnosed with metastatic PCa, and what have been your PSA readings since stating ADT? Hvae you had multiple scans to see the impact ADT is or isn't having on those metastases?
"... castration resistant means that the patient seems to be losing the battle with the current treatment?"
The phrasing could be better. When you become castrate-resistant on your current treatment, as shown by rising PSA or increasing mets, that treatment has lost its effectiveness.
Yes, regarding ADT.
Castration resistant does not mean the patient is losing the battle. Just because the patient is no longer responding to hormone therapy does not mean it is the end of the road. It means that a different road of different therapies must be taken instead. So in that sense, maybe it can be considered the end of one road and the beginning of another. Good luck
It means the cancer progresses even when the testosterone is below 50. Castration resistant cancer is lethal so it will kill the patient unless therapies can prolong life and the patient die from other cause.
The problem is that therapies may not work or fail rapidly.
For example my cancer does not respond anymore to castration levels of testosterone, does not respond anymore to Lu 177 PSMA treatment like when the cancer responded to castration, does not respond to darolutamide etc. The possibilitied of treatments shown to prolong life are going away.
Clinical trials is the way to go.
Anyway, I have survived 22 years (I'll be 80 in one month}) . since initial diagnosis of a high risk cancer witha PSADT consistently less than 2 months.
I have hope in science and willing to try new therapies, so the journey has not finished yet.
I came across this trial which is for PSMA negative patients: classic.clinicaltrials.gov/...
This super-abiraterone (ODM-208/Cypides) seems promising: classic.clinicaltrials.gov/...
Check arx517 or AMG 509 or epi-7386 from the top of my head…
Thank you
Thanks, I have been doing that, There are many. The problem is that most of the trials with new anti androgens are in phase 1. All of them do not allow moving to a cohort with a higher dose and they do not allow to participate in phae 2 or 3 if were in phase 1, which is understandable. The other thing is that the preliminary results are not very encouranging. Most patients do not rezpond and if they do the response is short lived for most of them.
The ODM 208 has a good response but one could develop Addison disease.
At this time it is a waiting game for me. Trying to contain the cancer until some of these trials start the phase 2 at least.
AMG 509 has very good preliminary results and looks like it will move to phase 2 soon, arx517 got the fast track from FDA, but yes I totally understand you !
Thanks, I have a peripheral neuropathy caused by an immune problem. Risky for me to participate in immunological trials or chemo trials as long as I can avoid them. I have only detectable lymph node mets at this time.
I appreciate your help. I have been in touch with the people running all those trials, so contacts had been made and I'll have to make a decision when phase II trials are going.
I prefer to try the new anti androgens, the protacs. There are several trials and I have had interviews with most of them. EPI-7386 is very difficult to qualify because of the requirements in relation to prior treatments. I hope they will change the design.
Thanks for your help, i really appreciate it.
Have you given Dr. Gary Onik a call?
No.
ok, just a thought for another treatment provider
Good Luck
Thanks for the suggestion Ivwas planning to look him up.
For BAT? I think you've mentioned him recently. If so, maybe I should contact him. Not quite CR yet, but the clock is ticking.
My BAT is an experiment on my own part with no guidance from elsewhere. Pretty sure that what I've been reading, BAT has been limited to men who are CRPCa.
Yes, thanks. In Denmeade's patient guide, he seemed to say that promising early results were had in limited trials when the patient failed ADT (before even starting Zytiga, Enza, etc.).
wow Tango! your journey gives hope to many men I'm sure!! I assume the referenced doubling time is fairly recently?
No it was the same in 2005.
Your PSa has had a rapid doubling time starting in 2005? PSA now??
The cancer progression has been stopped several times with different treatments.
I had prostatectomy, salvage radiation with ADT (whole pelvis radiation up to aorta bifurcation), vaccine treatment which stopped the cancer progression for 9 years., ADT plus Lu 177 PSMA in 2016 , ADT+ darolutamide, then further Lu 177 PSMA treatments etc. etc. I have been in ADT since 2016.
But everytime the cancer got/gets uncontrolled the PSADT was/is less than 3 months. The same PSADT I had during my first recurrence in 2004.
My last PSA was around 50, and we are trying to use other anti androgens and see what happens, meanwhile I try to get into a clinical trial.
I can't have chemo unless is the last resort, so we have plan for low dose cabazitaxel. We'll see if I can get into a trial soon.
I am interested in your course but you don’t include it in bio.. Did ADT work for more than 10 years?
God bless you Tango65! You are an inspiration to us all, and your mental attitude towards this terrible disease is nothing short of amazing! Thank you so much!
Thanks. I wish the best of luck with your treatments.
If your current hormone therapy is no longer effective and the PSA value rises, you can get a chemo or Pluvicto.
if your testosterone is near 0 and your PC is increasing as evidenced by PSA rise and or radio-graphic evidence you are castrate resistant by definition.
Hey Grant.
I am Castration resistant , It basically means that the Treatment, in your case Abiraterone mine enzalutamide is not working/Effective anymore.
Oh no, it is working. Its just the PCa cells are now adapting to being without Testosterone.
A fine distinction.
It is an interesting question and one that I have wondered about myself. I was on Lupron and Zytiga and failed so they called me castration resistant. Had mets everywhere including lymphs. Then I switch to Xtandi/Lupron (Eligard now) and zero PSA and all dormant mets.
So am I still CR? Even thought this current regimen is working?
Once CR, always CR? Thanks for the response. From the response of others I am guessing you are not but I find the vocabulary and scientific terminology daunting to say the least. Continued good luck.
Totally agree!! The terminology and abbreviations are hard to understand! I am slowly getting it now, but I do this for my husband and am not actually fighting the disease!
How do you know a met is dormant? Comparing PET scans over time or is there another way to know? Thanks.
I've been on Lupron only for 5+ years. During that time, PSA has spiked 50-75 % three times, then fallen back. Reading in December was 1.37 (up from .97 in September), reading on Friday was 1.27. we're monitoring, but "rising PSA" can be confusing without more specifics
ADT therapy by design is intended to induce a low testosterone levels, named "castrate". Same as if you remove your little friends down there, but instead of surgery, is done with drugs.
In this environment, the cancer is deprived of it's main driver. But like most cancers, eventually the cancer learns how to get around this. When the Prostate Cancer progresses, in the still low Testosterone environment, it is what you're asking about, or called "Castrate Resistant" because it is active despite the lack of it's driver. It moves on, has ridiculously expanded the number of T receptors on it's cell surface and even has been shown to produce its own... Crazy stuff!
Question is, what's next? Treatment to help keep the PCa controlled? Put the PCa back to sleep, kill it, etc. And some therapies have even been shown to "Reset" sensitivity, allowing the ADT to work again. Now, who are those patients and how do we identify what might work for that individual? Well, we aren't quite there yet, so we succumb to the SOC and till the dice, see if this or that works, all the while the PCa has free reign to do what it wants until checked!
Castrate Resistance is a scary place to be, but there are effective measures that have worked. Get to a Major Cancer Center and one rated in Excellence if you're not currently engaged with one providing your care.
Good Luck and Best Regards
Thank you so much. I suspected it was a term of art and I was not yet clued into its precise meaning. You provide an excellent introduction. I go to the VA and from what I have been reading here they provide the same SOC as everyplace else but without a lot of information or interaction with actual doctors. Best regards to you as well.
Hi Cooolone - great right up. May I ask what therapies have been shown to reset prostate cancer cells to ADT again?
Tall_Allen does not sugar-coat or generalize. His responses are based on solid data from credentialed sources.
This just means that you have been diagnosed with metastatic prostate cancer and are receiving treatment for it. If the treatment is no longer working, then your cancer might be castratio- resistent , and your medical team may decide to look for different treatment for you. As TA stated, they will know that your cancer is castration-resitent if your PSA starts going up significantly. My husband has been on the same medication since 01/23. So far, so good. Best of luck, my friend!
Castration resistant means precisely what TA wrote as succinctly as you can write it!!
I have seen several other definitions on here that may lack the brevity but more than make up for it in clarity.
This may be an oversimplified analogy, but I compare it to antibiotic resistance.
We know today many bacteria are becoming increasingly resistant to treatment with antibiotics to the point where some antibiotics will no longer kill those bacteria.
Same thing with prostate cancer cells and ADT. At some point, just like the bacteria, the prostate cancer cells build up a resistance to the ADT/reduced testosterone (castration) and the cancer continues to grow again. That's castration resistant.
I like it (the explanation.) Thanks for helping.
I was put on lupron when my Psa hit 5664. It came down to 6 and then started to rise. As soon as it started to rise I was considered Castrate resistant. I then went on low dose abiraterone and Psa is still dropping. Even though I am castrate resistant which was demonstrated by Psa rise while on lupron, I am still hormone sensitive because Psa is going down while taking abiraterone. Hope this helps.
Thank you so much. I assume you are still taking the lupron. May I ask the parameters of low dose abiraterone?
Sorry for the delay. 350 calorie with low fat. Mine is a cup of cereal with blueberries and a half of a banana. I take my 5mg prednisone at the same time as I take the 250mg abiraterone. If you google low dose abiraterone/ Rutgers Cancer Institute you will get a page with breakfast suggestions.
my aberaterone bottle says take 2 hours after eating and then wait one hour before eating
Pred says take with food ..seems you cant take them together ?
Sorry I now read Rutgers try to reduce dose with food…if I have side effects with fulll dose will consider
I don’t think low dose will reduce side effects unless it would be nausea. You take less but get more absorbed because you take it with food which is why I take prednisone with it.
I take 500 without getting the horrible coughing side effect but in the standard way, after fasting and an hour before food. I wish I could find someone who did this successfully, lol. It sounds as if your method is working. Stay well.
yes I am still receiving Lupron injections.
Thanks for the help. First I have heard of this.
I don't think the prostate cancer cells "learn" to survive with ADT, it's more like the type of cells that resist ADT survive better and eventually overcome the treatment, causing PSA rise or metastases. There are dozens of types of prostate cancer cells.
TA's definition is good, imo.
Getting more to your question, if you are castrate resistant it would be evident from a rise in PSA during/after hormone treatment.
yes, it's an evolutionary process, driven by the fact that there are tens of thousands of new cancer cells daily, some of them may have a random mutation that brings a survival advantage, at that point they are fitter for the environment, you are right: "learning" is a verb that underlines a conscious process, this is not conscious, just based on big numbers and probability 
....all the treatments we do put some kind of evolutionary pressure on cancer because we kill what we can kill but leave the door open to other kinds of mutated cells, people trying BAT are trying to avoid that for example
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