Xtandi a second line anti-androgen is approved for mCRPCa..if you are not metastatic Medicare won't pay. Now the FDa has Apalutamide on Fast Track for non-matastatic CRPCa with Doc's hailing the unmet need for this drug. These idiots know full well Xtandi would have worked equally well for non-metastatic CRPCa. So let me get this straight...I am diagnosed with PCa...have a RP...RP fails with BCR...put on Lupron which causes Castrate Resistance which allows me to qualify for Apalutamide if there is no metastasis and Xtandi if there is metastasis...so the key is Lupron...I have to get my hands on Lupron fast so I can become Castrate Resistant.
Gus
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gusgold
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I agree, it's really ridiculous. I blame the drug makers who are looking for the bigger market. "Early use" seems to be what they are looking for. The trial for Darolutmide is another "early use" trial so the CRPC patients who really need it most won't have approval.
PC becomes castration resistant whether one takes Lupron or not. In fact, the selective pressure of Lupron has been found to be outweighed by its reduction of the volume of metastatic cells. Castration resistance occurs more quickly among recurrent men who do not take Lupron than among those who do.
Apalutamide was just the first drug approved for non-metastatic CRPC. I expect that Xtandi will also be approved for it shortly.
Non-metastatic CRPC is a relatively rare disease. For most men, metastases are discovered before CR sets in. In the studies for the new indication, men were only enrolled based on lack of metastases on bone scan/CT. With Axumin and the experimental PSMA-based PET scans, I doubt they would have found any non-metastatic CRPC at all.
I don't agree at all...was told by Onco's at the Mayo Clinic I will not become castrate resistant unless I take a Drug like Lupron to lower T to castrate levels
Dr Duchesne (the lead investigator) wrote: "One of the most thought-provoking findings was that the development of the castration-resistant phase occurred significantly earlier in the men who started treatment after a delay, a counter-intuitive finding. This may again be linked to treating low volume disease before it grows resistant clones."
that is one worthless study....there are studies showing no OS benefit for ADT. Dr. Myers...Dr. Strum...Dr. Leibowitz all advocated 13 months of ADT3 and then never go on ADT again to delay the onset of castrate resistance...ADT selects for the cancer cells that can thrive with very low levels of T. You do the ADT and and I will do anything I can to avoid it after the 13 months of initial therapy.
Maybe you would like to post your study to refute your claims Gus. I am just a little confused , If it has no overall survival, why would they prescibe it at all. I am pretty sure they would be referring to patients with no evidence of disease, and undetectable psa after 13 months stopping adt, and if psa never got to UD they would not stop adt. I also believe Tall Allens study and think that untreated metastatic Prostate cancer mutates . I guess we all have our point of views, and some have peer reviewed papers to back it up.
Because it is a palliative treatment....I just watched a 2017 video against the early use of Lupron stating the massive side effects and no proven OS benefit because of accelerated CR...also you are making the same false assumption as TA...I did not say not to treat mPCa...I said there are better drugs than Lupron that do not lead to early CR.
I did think you were saying that, What are the better drugs, perhaps firmagon. Gus you have done well to have never needed androgen suppression for more than 4 months in this disease, many of us not so lucky, and never achieved such a low psa. What was your original presentation? You know my history, I have been predomitely CR since the start in 2006 at age49.
So you don't want to let facts get in the way of a firmly held opinion? ADT3 failed when it was tried in a randomized clinical trial. Anyone can formulate a hypothesis, but whether it is true or not can only be proven by an RCT.
you just said early ADT improved overall survival..now you are saying ADT3 failed... there are studies showing ADT3 is superior and studies showing it is not...any researcher can design a study to obtain a desired result. Also you are comparing early use of Lupron to no treatment...I said to delay Lupron not to delay effective treatment...Dr. Myers said he lost more men to side effects of lupron than to the PCa itself. I had 4 months of Lupron and never went on that poison again controlling the PCa with other drugs...10 years out...no castrate resistance and PSA never higher that .3
I think you're both right in your own way. I think it is now believed that virtually everyone's PC c contains both cells in high numbers that are castrate sensitive, and low numbers that are castrate resistant. We start off with both. The Lupron kills off large numbers of the castrate sensitive ones initially, it makes others go I to a sort of homeostasis and remain inactive for some time, and the small number of cr ones survive and multiply over time. The percentage of low number castrate resistant cells to start with may be fairly uniform, but if someone has highly advanced PC at diagnosis and a spa of say 500, they are likely to already have a much higher number of castrate resistant cells than someone with a spa of 5 at diagnosis. Therefore, once on Lupron, the volume of castrate resistant cells will more quickly be identified through imaging or physical symptoms of metastasis, than with a patient starting on Lupron with a very low morph load. Much of this info is from what I have found in research, some is from fairly intuitive conclusions of my own. I hope this helps a bit.
you are right...the key fact is high numbers of CS cells and low numbers of CR cells. The cancer has limited resources and by killing off the CS cells, with lupron, you are taking away the competition for those resources. The 2004 study referenced by TA was not even Double Blind rendering the conclusions virtually useless ...like the study that eating fish promotes aggressive PCa.
It was a 2016 study, not 2004. It could not possibly have been double blinded, or even single blinded, because the deferred therapy cohort had to be taking, you know, nothing. It would be unethical if a patient in the deferred group had rising PSA or detected mets and the doctor could not tell whether he had received ADT or not. Many RCTs can't be blinded - that does not invalidate them.
There you go again ...the study start date was 9/2004...if the patient had received ADT what was the purpose of the study...not double blind = worthless
You haven't seen many research studies, obviously. Either that, or you're being intentionally obtuse - in which case I won't bother trying to correct the misinformation you believe in spite of all evidence. They began recruiting in 2004 and continued through 2012. Data collection continued through 2014 and it was published in 2016. This was a recent study. Even the earliest recruits had available to them all the same hormonal therapies that later recruits had.
The cynical response is that the makers of the new drug looked at the market and the state of Zytiga and Xtandi. Those 2 drugs pretty much had the mCRPCa sowed up by the time Apalutamide was ready for trial. So go after the untapped market. Good business choice as trials are slow and very expensive. Maybe not such a good choice for us.
FWIW, I was on Eligard for 12 months after a robot assisted prostatectomy prompted a diagnosis of "very aggresive PCa" and showed involvement with all the stuff they pulled out - prostate, seminal vesicles, lymph nodes, and nerves. PCa was 1.9 after surgery, dropped to undectable after Eligard. Dr. said to try a vacation, which did not go well. PCa was 2 something at first test after vacation start, then 10 something at second with a doubling time of about 2 months. But no new mets showed on a scan. Back on ADT, but Trelstar this time. PSa dropped to undetectable again. Have been on ADT for 4 years straight (plus a few months) with undetectable PSa continuing.
My conclusion about my particular case? I would be quite dead without the ADT. I am still castrate naive. I hope to stay that way a long time. I will take my chances with ADT since it seems to be keeping me alive.
Beer maker have you thought about taking a breaks intermittent holidays since that first one or did you just give up on holidays and stay on it continuously?
Also have you thought about adding zytiga and prednisone to extend the castrate resistance time period?
“I don’t want to say this is the best thing since sliced bread — it’s not,” said Dr. Oliver Sartor, medical director of Tulane Cancer Center. “You’re taking a person with no symptoms and potentially giving them side effects, definitely giving them an expensive drug. And it is unclear if this is the optimal management of these patients.”
The current list price of enzalutamide is more than $10,000 a month; a price hasn’t been set for apalutamide, which is not yet on the market
Dr. Sartor and others noted that another androgen receptor inhibitor, abiraterone, which is used to treat cancer once it metastasizes and is also produced by Janssen, is likely to go off-patent soon and will become much cheaper because generic versions will be produced. Since abiraterone operates on the same biological pathway, experts expect that it will be tried for patients with cancer that hasn’t metastasized and could end up working as well.
Now that the PROSPER trial has been published, I would expect Xtandi will be approved soon. prnewswire.com/news-release...
Have your Medical Oncologist write a letter. I ran into the same with no testosterone script due to my prostate cancer. Some non-physics need is making the decision. Always have Physician talking to Physician.
This discussion thread is interesting but a lot of these questions about what people should do has a lot to do with how aggressive the cancer is. Doubling time doesn't get mentioned enough.
I'm not sure what how direct of a correlation there is between doubling time of the PSA and longevity or doubling times relation to the effectiveness of the Lupron and other ADT treatments but I do know that when I took a Lupron holiday and my doubling time is three weeks. meaning that I go from 0.1 up to 10.8 in a matter of a few months then it doesn't make any sense for me to consider some of these arguments about not taking ADT after 13 months. what am I supposed to do let the PSA just rise up to a couple hundred or even a thousand? that's certainly not going to do me any good.
I have often wondered though, is there a direct correlation between psa doubling and longevity for people using lupron. I know what the John's Hopkins prediction table show but I wonder if those are based on people who may not have been using lupron, zytiga etc.
Heck, Michael Milken is still alive and supposedly he just does intermittent lupron and got imrt radiation like twenty years ago with a Gleason score of nine, presumably with a fast doubling time.
doubling time is crucial...a DT under 3 months is a fatal cancer if not treated...the argument is to do ADT3 for 13 months and then control the cancer with drugs other than Lupron to delay CR. Because of his money and funding for PCa research, Milken, has access to all the cutting edge treatments even before they are approved. You can correspond with Milken by email through his foundation, I have, and he is way beyond soy and Lupron..though I am not at liberty to disclose what his current treatment is
No one said not to use ADT...the discussion was if Lupron hastens the development of CR. ADT stands for Androgen Deprivation Therapy...by that definition Zytiga or Xtandi would be ADT...either drug deprives the cancer of T...my Onco at Mayo Clinic uses both Xtandi and Zytiga as stand alone treatments when they are covered by insurance...An Onco at The Cleveland Clinic told me he favors Xtandi over Lupron/Zytiga if the patient can get the $10,000 a month covered by Ins or one of the programs that pays the cost of the drug
The first drug I was on is casodex. Once casodex stopped working I was considered to be castrate resistant. I went on to nilandran and then flutimide. The point is, I then was eligible for an aboratorone trial and then an xtandi trial. Both trials required that the subjects did not have had chemo (taxotere), and be castrate resistant.
Whether xtandi or aboratorone and are given to non-castrate resistant patients I am sure. I would think "Big Pharma" would prefer their customers take a cheaper drug like casodex or Lupron before having to pay for xtandi or aboratorone.
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