I remember Dr. Myers being cautious regarding Zytiga vs Xtandi. He said that he generally preferred Xtandi because he said in 25 percent of the cases Zytiga could aggravate the cancer.
My notes from that visit are " "In 25% of the cases Zytiga makes prostate cancer more aggressive"
I have not seen anything about that in this forum though. Given that generally you must choose one or the other, it would seem that if this were true, Xtandi would be the easy choice.
1. Does anyone have any information on the pros and cons of Zytiga vs Xtandi?
2. If your Doctor chose one over the other, did they ever indicate why?
Written by
cesanon
To view profiles and participate in discussions please or .
I was on Xtandi monotherapy for 8 months . Zytiga requires concrruent use with a steroid. Private message me if you want to know about my Xtandi experience. They are all good as far as I have heard.
I have been zytiga + prednisone in a trial. Zytiga worked for 3 1/2 years. I am now on a trial with xtandi + a mystery drug from Johnson and Johnson. It's been 3 and 3 1/2 years for xtandi. Each of these drugs works in a different manner and the side effects are about the same. So don't dismiss either.
I would guess if you were one of the 25% in which Zytiga allegedly causes the cancer to go aggressive, your Doc would figure it out pretty quickly and alter course?
My dad was on Xtandi for 3 months under Dr. Myers' care, and the side effects were horrific, it almost killed him (very noticeable neurological effects, stopped eating, couldn't move). Myers switched him Zytiga and he went on a 5 year durable remission, till he died from the stroke.
I’m pretty sure Xtandi passes the brain blood barrier. Compared to Zytiga I had worse SEs from Xtandi. More brain fog , fatigue and it aggravated some restless leg syndrome I had. I also developed a bad floater in my right eye. Caused by Xtandi not sure but it went away shortly after I stopped using it.
I take 80mg of Xtandi at bed time . Started with 160mg it really messed me up! Went down to 80mg still not good! I go to bed at 8pm sleep till about 2am then toss and turn for 3 hrs then fall back to sleep till 6am. I get pains in the head can not focus like before, loose interest, always tired, etc. can't take much more of not being my self
I think he guessed wrong as often as he guessed right. Unfortunately, he preserved his wrong guesses in outdated youtube videos that patients, who haven't kept up, take to be still true. Logic only gets one to a hypothesis - a clinical study is the only proof that counts.
Indeed, Dr Myers is correct that Zytiga can cause a virulent, "treatment-emergent SCNC" (small-cell neuroendocrine cancer), clinically different from de-novo SCNC. About 20% of those treated with Zytiga develop this form of PCa.
Zytiga causes "treatment emergent" SCNC in 20% of CRPC cases, why would I risk a mutation to small-cell PCa if Lupron is doing the job with T: 1.5 and PSA: <0.01? I am not CR, but still don't want to risk it unnecessarily.
But what is the association of small cell cancer with Lupron?
Maybe it is just the natural progression of regular prostate cancer in 15-20% of the cases.... and is not associated with Zytiga and Xtandi and more or less than with Lupron.
By the way I just discovered that Eligard is superior to Lupron in one respect. It is injected into fatty tissue as opposed to muscle and as a result maintains more stable levels of leuprolide acetate than do Lupron injections. The one disadvantage is that it appears almost no insurance covers Eligard.
For us skinny guys with very little if any belly fat, Eligard (Firmagon) is going to form a painful welt - lasting for 4-5 days. It is like being stung by a dozen wasps on one concentrated spot! Even though my insurance pays for Eligard, I have gone back to Lupron.
What is your secret to staying skinny on Lupron? I have always been very active and kept my weight between 175 and 180 for the last 25 years. I am 6' tall and now 72 years old. Had PC since 2002 but only had to start Lupron in February. I eat very healthy and very little. I lift weight 2 times a week, walk 2.5 miles 2 days a week and play golf 2 times a week. However, I have gained 10 pounds that I can't get rid of. What is your secret?????
I lost 50 pounds over the last three months (250-200) by eating mostly plant based foods and posting my meals and calories burned on an app “my plate”. I’m 6’3”. I limited calorie intake to 1250/day and burn 300-500 by working out so net calories are 700-900/day. I also stopped standard ADT and went on estradiol patches but that’s not to lose weight but to reduce side effects.
You misinterpreted that. Zytiga does not cause SCNC. By killing off the normal acinar adenocarcinoma and leaving the SCNC untouched, it allows the SCNC that is already there to dominate (which it will do anyway). Progression to CR is delayed in men who take abiraterone for mHSPC, and survival is increased. SC is very rare in men with HSPC, and is still uncommon (but up to 17%) in men with mCRPC. You can test for SCNC to allay your fears, but it is very rare in men who are not CR.
No, two distinctive subtypes: natural and tx-emergent, Zytiga is associated with the later.
Rahul Aggarwal et al note the “substantially higher” prevalence of t-SCNCversus de novo SCNC – thought to occur in less than 1% of prostate cancer patients – and suggest this “may reflect a transdifferentiation process after androgen-ablating therapy.”
I read that as Zytiga is associated with a mutation of adenocarcenoma to the t-SCNC subtype.
No. You are misunderstanding the subtypes. "de novo" means that the patient is originally diagnosed with SCPC - occurs in <1%. "Treatment emergent" means he detected it in heavily pre-treated patients, and it occurs as a mixed type. It does NOT mean that the treatment in any way caused the SCLC. In fact, the reason that the mixed type is occurring more often now is only because men are living longer with their PC because of the treatments now available. To forgo those treatments (like abiraterone) might mean you are less likely to be diagnosed with t-SCNC because you will die before it can be diagnosed.
I don't know how you interpret this as not causative:
“We think it arises from [the original] adenocarcinoma," Dr. Aggarwal said. "The cancer cells transform into this subtype of prostate cancer through genetic reprogramming.”
Some aspects of this reprogramming event are understood, such as specific factors that control the transition. However, he added, “more studies still need to be done to understand how and when it happens.”
Potent hormone therapies such as abiraterone and enzalutamide may push prostate cancer toward this transformation.
I understood there is a natural subtype, "de-novo", and the one caused by Zytiga.
You misunderstand the natural progression of cancer. Genetic breakdown (reprogramming) is part of what happens naturally, whether you do any therapy or not. Selective pressure does not cause SCPC. The cancer itself mutates naturally into it. It is discovered in heavily pretreated patients more now simply because they live longer because of those treatments.
Imagine two normal PC cancer cells. After abiraterone treatment, one mutates into, say, an abiraterone-resistant subtype, like AR-V7. The other mutates into a small cell (SC) subtype. Let's suppose that after docetaxel treatment, the AR-V7 cell is destroyed, but the SC cell survives. The SC then proliferates. You would not conclude that docetaxel caused the SC.
Zytiga is one of the most life-prolonging medicines we have. It does not in any way cause SCPC, and Aggarwal does not make that claim - that is just your misinterpretation. I suggest you discuss this with your oncologist because your misinterpretation is dangerous to your survival.
As I thought about it, I realized that you are also confusing association with causation. Zytiga has been proven to extend life after chemo, before chemo, and in men who are mHSPC. There is proof of a causal benefit because extensive randomized trials have been conducted. That is the only way to prove a causal relation.
What Aggarwal did was detect an association between heavy pretreatment and SCPC. Heavy pretreatment did not cause SCPC, it was only associated with his detection of SCPC. To determine cause, he would have to have two groups of men with mCRPC - one given abiraterone, the other given placebo. If the abiraterone group died sooner, it would prove causation. In fact, this has been done already, as I mentioned above. What it proved was that abiraterone extended survival. Even if abiraterone caused SCPC by some unknown mechanism, as you suggest, the effect is not sufficient to negate the overall survival benefit of abiraterone.
TA, you're coming to the wrong conclusion because you're grouping the de-novo and t-SCNC subtypes, however,
(1) they are genetically different, and t-SCNC is strongly associated with Zytiga tx.
(2) median OS of mCRPC men is shorter for men with t-SCNC.
(1) ...messenger RNA sequencing was used to group tumour samples into five different clusters depending on the expression of 528 genes. In all, 43% of the 14 pure t-SCNC tumours fell within cluster 2 compared with just 26% of seven tumours with mixed histology and 4% of 90 tumours that were purely adenocarcinoma, a significant difference.
(2) Median time from the development of metastatic CRPC to death was 42.1 months; median overall survival (OS) among patients with a history of abiraterone and/or enzalutamide use was significantly shorter for men with than without t-SCNC (36.6 vs 44.5 months, hazard ratio [HR]=2.02).
There is no doubt that men with SCPC have shorter survival than men without it. That has nothing to do with causation - it's just an observation. I would similarly observe, for example, that there are any number of genomic mutations that shorten survival. You are confusing cause and effect. The fact is that abiraterone lengthens survival:
In men who are mHSPC: 53 months vs 36 months
In men who are mCRPC and have not had docetaxel: 35 months vs 30 months
In men who are mCRPC and have had docetaxel: 15 months vs 11 months
So why would anyone in his right mind forgo abiraterone?
You will note that men who have had docetaxel survive significantly less than men who haven't. Using your backwards logic, men would be better off not having docetaxel. It is backwards because they had docetaxel because their disease was further progressed. I think you see how reversing causality leads to erroneous conclusions.
I'm not debating the overall benefit of Zytiga, that's well known. What Dr Aggarwal did is a prospective study showing that 17% of mCRPC using Zytiga wound up with t-SCNC. Further, those with t-SCNC had a shortened OS with a HR of 2.0, and , meaning those on Zytiga that developed t-SCNC were twice as likely to have a shorter OS. Further, he went on to uniquely differentiate t-SCNC from de-novo small-cell neuroendocrine carcinoma (d-SCNC) which only occurs in 1% of mCRPC patients.
Semantics aside, that's suggestive of causation, or in statistics, "causal interference", if one group not treated with Zytiga has a 1% chance of d-SCNC, versus another group treated with Zytiga has a 17% chance of t-SCNC, with a HR of 2.0.
So that means the benefit of taking Zytiga for mCRPC patients to gain an overall survival benefit comes with a significant risk of developing a form of SCNC (t-SCNC), that is twice as likely (HR: 2.0) to shorten median O/S by about 8 months (44.5 v 36.6 months).
All he is doing is observing that prostate cancer has "unique histological subtypes." Some of those subtypes lead to different resistance pathways. Some lead to resistance through DNA repair mutations, some lead to resistance through changes in the androgen receptor, what it requires for activation, its amplification, and its translocation to the nucleus. He is adding t-SCNC to the list of known resistance pathways . All of the resistance pathways are prognostic for shortened survival, but t-SCNC is particularly virulent. He is not saying that t-SCNC can be avoided by avoiding Zytiga. He can't make a causal inference because all of his evaluable patients had failed Zytiga or Xtandi and there were none evaluated who had not already tried Zytiga or Xtandi. He would need to compare those groups to even suggest a causal effect. He would have to do a randomized trial to prove a causal effect.
Let's review what you wrote:
"Zytiga causes "treatment emergent" SCNC in 20% of CRPC cases, why would I risk a mutation to small-cell PCa if Lupron is doing the job with T: 1.5 and PSA: <0.01? I am not CR, but still don't want to risk it unnecessarily."
The conclusions you draw are not warranted by the study he did, and may be injurious to your health. All three studies that prove the benefit of Zytiga (that I showed above) prove that you are better off taking it than not taking it. I suggest you discuss this with your oncologist before taking any rash action (or avoiding a beneficial action)that may harm yourself.
True, statistically speaking, because this wasn't a randomized study, I can't say Zytiga "causes" t-SCNC, but you can't say Zytiga "doesn't cause" t-SCNC either. But,what this observational study shows is a statistical inference that the chances are 1:5 of a mCRPC patient on Zytiga developing t-SCNC and a resulting shorter OS.
So what if there are a few small-cell NE cells lurking in my body, and I take Zytiga, couldn't it be inferred that the chances are 1:5 of those NE cells mutating to t-SCNC whether I'm -m or -nm, -CR or -HS based on this statistical inference ?
You are trying to make something causal when there is absolutely no evidence for it. Let me tell you a true story... Several years ago, researchers at Johns Hopkins noticed that a small proportion of men taking abiraterone and enzalutamide failed it quickly and their survival was lower. (sound familiar?) Genomic analysis revealed that they had a mutation of their androgen receptors, which they called "the AR-V7 splice variant." This was just something that their tumor had mutated to. It wasn't "caused" by abiraterone or enzalutamide, but the mutation caused those therapies to fail quickly. They now have a CTC test for it, but why pay for the test? Just take Zytiga and see how long it lasts. This is very similar to the t-SCNC situation that Aggarwal identified. Do you see that now? It is not a reason to avoid taking Zytiga, it's just something that may occur in about 17% of men who have already tried chemo and Zytiga for mCRPC. The opportunity, as with the AR-V7 splice variant, is to identify the biochemical pathway that causes that mutation, and to develop a new drug that interferes with it.
"You are trying to make something causal when there is absolutely no evidence for it."
Not really, I'm trying to make an educated decision based on a statistical inference. I would rather make a decision based on less-than-perfect information (observation study) than waiting for perfect-information (randomized study) that will never happen.
I totally understand that causal relationships require randomized studies, but I have to make the decision now based on what studies are available. If I see a study that infers a strong relationship between Zytiga and tSCPC I have to consider it, even though it's observational.
Further, the quandry I have is, none of the studies about Zytiga include my prior treatment and pathology. For example, HDR-Brachy is exclusionary for studies like Stampede. The majority of Stampede entrants were Gl => 8, I'm Gl 7. Also, M0 is exclusionary for studies like this one Aargawal did.
So let's say, I walk into your office as a MO with prior HDR-Brachy, IMRT, Lupron for 9 months, and T: 1.5, PSA < 0.01, would you recommend Zytiga?
I suggest you look up "statistical inference." It doesn't mean what you think it means. It does not mean that you can infer a causal relation from a mere association. If taller people are more likely to be murderers than shorter people, one can't infer that height causes homicides.
In your example, what is the evidence that you haven't been cured? Why would you be taking anything if there is no evidence of recurrence?
I know enough stat to be dangerous, but what I do know is that a random trial can determine a causal relationship, but an observational trial like Aggarwal did does not, but it can provide a statistically valid inference that a drug or treatment affected one group differently relative to another (the HR ratio). In this case, with a HR: 2, CI: 1.07-3.10, p: 0.027, it is statistically valid that the patients taking Zytiga represented 20% of the population and were twice as likely (HR: 2) to have a shorter OS (median of 8 months.)
My wife is a clinical researcher, and I asked her if I can say "statistically inferred" in an observational study? She said no, that the wording should be "associated" or "correlated", and the measure of association is the HR ratio. So, yep, I was a loose canon with the working "causes". Then I asked if treatment decisions can be made on observational studies, and she said yes, if statistically valid and the HR is high enough, trends or associations can give clinicians a reason for a treatment decision.
In your example, what is the evidence that you haven't been cured? Why would you be taking anything if there is no evidence of recurrence?
I may be cured by the HDR-BT and IMRT alone. Nothing indicates I'm not. One study I saw, that chances of remission were low if going into IMRT PSA were <0.6, and mine was <0.1, and now four months later, <0.01. Thankfully, I started ADT two months before radiation, which successfully pulled my PSA down into that favorable group. Scholz was pushing me for 4x Taxotere, which I decided definitely not to do since HDR-BT is exclusionary for Stampede and the other trials. Then, I took a risk, and personally dropped Zytiga because of high BP, and don't see a reason to go back on it with T: 1.5 on Lupron, and being wary of t-SCNC from Aggarwal's study. I'll probably just finish out 9 more months of Lupron, stop treatment, and see what happens.
You misinterpreted that. The hazard ratio (HR) is not between patients who took abiraterone and those who didn't. It is the hazard ratio for men with the t-SCNC to die in that timeframe compared to those who don't have t-SCNC. In other words, if you have the t-SCNC mutation, you were twice as likely to die in that timeframe compared to those who didn't have the t-SCNC variant.
It was not in any way a comparison between those who took a second-line hormonal and those who did not, as you imagine. In fact, look at Table 1. In the first column, you will see the words "neither abiraterone nor enzalutamide." For ease of interpretation, let's look at the inverse (the percent that took at least one) -- so 74% of those with 27 men with t-SCNC had taken at least one of them, and 68% of those 133 men who did not have t-SCNC had taken at least one of them. Now, over to the right, you will see that P for the interaction is .789. That means you reject the hypothesis that there is an interaction effect. It did not make any statistical difference whether they took one of the second-line hormonals or not.
If you will listen to your wife, have her read this.
I agree with your decision to not have a second-line hormonal, but not because of Aggarwal's study. The reason Scholz was offering very aggressive medicines like docetaxel and abiraterone adjuvant to brachy boost is because he is a medical oncologist who specializes in treating incurable cases. If you were under the care of a radiation oncologist, whose job it is to know what works with radiation and what doesn't, I doubt you would have had that recommendation. There is no evidence that taking anything more than 18 months of adjuvant Lupron will help much.
So here’s how I view this whole scenario. You are both sort of right! Let’s first assume that SCPC will occur from de novo regular pc at some point... as Tall states. That assumption sounds reasonable, though I don’t personally know if it’s been clinically proved. But let’s accept it as true. Is possible also that the newer AR treatments like Xtandi and Zytiga will push the evolution to SCPC along quicker. Unfortunately, this is something that has not, to the best of my knowledge, been tested. It is an area of clinical trial testing that is made quite difficult... because a majority of people who have CRPC and don’t get an AR blocker will die relatively if there are other limited options. It is this fact that I think reigns supreme. There are major risks to most PC treatments. Radiation and chemo can both lead to serious secondary cancers or a host of other side effects, but we use them because they improve survival time. So, if one has good alternatives to AR blockers, like PARPs in a trial or other trial drugs, those could be an alternate first start for CRPC, otherwise, the traditional AR blockers are still a great first choice.
Nope, read it in a clinical trial paper that the chemo can damage dna, thereby raising the potential for secondary cancers to arise, unrelated to the original cancer. The dna damage is even more concerning if the individual has dna repair deficits, such as myself. If you don't have repair deficits such as P53 or BRCA1/2, the chance of such harmful side effects is greatly reduced.
I recollect some sort of ground breaking mathematically based research that was clinically verified.
It said that when you got cancer you hit it hard and kill as much of it as possible. And you avoid multiple lesser attacks which will have the effect of generating a stronger evolutionary response.
I believe this concept has been clinically verified?
Of course more specific clinical trial results should always prevail over less specific clinical trial results.
But still, shouldn't this raise a few doubts here? Should it not require a few more trials before we jump to conclusions?
Ta, do we already have those multiple trials? Or do we have just one such trial?
Hirsch: Yes, Dr Aggarwal does practice at two San Fran clinics, one is the STAND Clinic (Supportive Therapy in Androgen Deprivation). It would be interesting to know his stance on Abi after his study. I may visit him next time I'm up there.
T_A I found this whole thread to be very educational for me. Thank you for your logically grounded and research supported contributions.
Going back to the original question Re: Zytiga vs. Xanti first. I am interested in a more practical angle: Rather than one or the other until you die. Is there any support for selecting a sequence such as 1) Zytiga until failure and then Xanti; Vs. 2) Xanti until failure and then Zytiga?
"The Dream Team detected small cell carcinoma in approximately 15-20% of post abiraterone or post enzalutamide patients. They were found in the lymph node, bone, liver, not selective for any specific metastatic site. So, while it’s not the only way the disease can progress, it is a reasonably common one."
17% of heavily treated mCRPC patients were detected with it. It has nothing to do with Zytiga, other than Zytiga kills many of the normal PC cells, leaving the SC behind (this is true of radiation, chemo and every other hormone therapy). Fortunately, it is very rare in men who are mHSPC.
To be clear, Zytiga is associated with its own small-cell neuroendocrine cancer (SCNC) subtype that's distinctive from the natural occurring type:
1) "de novo" Small Cell prostate cancer, which has nothing to do with ‘classic’ prostate cancer such as high PSA, sensitivity to ADT and taxane chemotherapy, and
2) "treatment-emergent", which occurred more often in the 200 size sample (27%) while the patient took abiraterone and prednisone.
#1 is a natural progression and would happen anyway regardless of ADT tx, and
#2 is Zytiga induced progression, which was more common in the selected sample.
I don't know of any studies thus far, but it's been identified by the NCI.
Sorry, I momentarily had "target-fixation" on Zytiga, because that's what I was taking.
I think the takeaway is buyer beware. The second-line ADT's evidently cause pressure on the PCa to mutate into a small-cell NC sub-type. There are many unknowns, so I wouldn't be alarmed, but I would discuss with your MO.
Dr. Aggarwal and his colleagues are investigating how the t-SCNC subtype develops in men with metastatic castrate-resistant prostate cancer.
“We think it arises from [the original] adenocarcinoma," Dr. Aggarwal said. "The cancer cells transform into this subtype of prostate cancer through genetic reprogramming.”
Some aspects of this reprogramming event are understood, such as specific factors that control the transition. However, he added, “more studies still need to be done to understand how and when it happens.”
Potent hormone therapies such as abiraterone and enzalutamide may push prostate cancer toward this transformation, said Dr. Dahut. That may be why this subtype is more prevalent in men who have received treatment than in men with newly diagnosed prostate cancer, noted Dr. Aggarwal.
The research team’s ultimate goal is to find therapies for t-SCNC. Master regulator proteins are opportune drug targets, Dr. Aggarwal explained, because they control many pathways that contribute to cancer growth and survival.
Cesanon: In the article I linked, read the two examples of patients: #1 had typical small-cell PCa which is termed "de-novo" subtype, naturally occuring. #2 had the subtype associated small-cell cancer treated by Xtandi referred to as t-SCNC.
"Under the microscope, t-SCNC looks quite different from adenocarcinoma: the cells are smaller and more crowded together. And compared to adenocarcinoma prostate tumors, tumors of the t-SCNC subtype are thought to have less hormone signaling and lower prostate-specific antigen.
In addition, t-SCNC shares some features with a small-cell neuroendocrine(de-novo) subtype of prostate cancer that appears in less than 1% of men with newly diagnosed prostate cancer."
In addition, messenger RNA sequencing was used to group tumour samples into five different clusters depending on the expression of 528 genes. In all, 43% of the 14 pure t-SCNC tumours fell within cluster 2 compared with just 26% of seven tumours with mixed histology and 4% of 90 tumours that were purely adenocarcinoma, a significant difference.
"'The cancer cells transform into this subtype of prostate cancer through genetic reprogramming.' ... Potent hormone therapies such as abiraterone and enzalutamide may push prostate cancer toward this transformation, said Dr. Dahut."
While treatments certainly select for & against existing cell variants, adaptations involving transformation do occur & one should expect higher levels with more efficient treatments. Dr. de Bono has expressed concern that we are ill-prepared to deal with PCa that is resistant to Abi & Enza.
That's probably because it is so rare. It can be easily tested for in biopsied tissue. Other clues are lytic bone mets, and PC unresponsive to normal therapies - radiation, chemo, and hormone therapies.
Docetaxel prolongs life more and has fewer side effects if it is used earlier. Many men have unwarranted fears based on others experience with different kinds of chemo for different kinds of cancer or used when it was already too late to do much good.
But what if other choices stopped working? The cancer itself kills the person sooner .I remember when my Dad diagnosed with advanced prostate cancer he had systemic symptoms he couldn’t breath,Walk or eat he was about to die if he wasn’t diagnosed and start treatment ,again after becoming resistant to ADT his symptoms and near death experiences came back abiraterone ceased the disease and gave him 10 more months to live. I think for super advanced prostate cancer patients there’s no other choice unfortunately
Annie, you’re right, in late stage advanced PCa, abiraterone is absolutely worth a try, it’s great your Dad responded to it and lived 10 more months.
This consideration really applies more to intermediate risk hormone-sensitive patients on mono-ADT that may not need to take Zytiga to reach low-T and -PSA, who want to avoid the risk of developing a more aggressive subtype associated with Zytiga.
My MO put me on Darolutamide since my liver enzymes were high from Abiraterone. Daro is not FDA approved for hormone sensitive PC but my MO thinks it is the best drug for HSPC since it doesn’t pass the blood brain barrier (fewer cognitive issues) and she said it works better on some of the mutations. Anybody else hear this from their MO?
It has only been FDA-approved for non-metastatic castration-resistant PC - It hasn't been FDA-approved for metastatic hormone-sensitive PC. You must have very good insurance.
My insurance is pretty good. Also, my MO seemed to know how to get it paid for. They also approved payment for Enzalutamide before it was FDA approved for HSPC but fortunately Darolutamide became available before I began taking the Enza.
I knew it was coming...Zytiga is generic now and cheaper so they are going to come up with fake studies to defame it. I mentioned and predicted this many months ago.
Its shame that as soon as a good medicine goes generic ..all the bad effects of it are advertised.
When they were selling Zytiga for 15 years at the price of $9500 a month, zytiga was gold and great. I do not believe these bought researchers who act like pimps for big pharma.
Zytiga is a great medicine..do not let false propaganda against it mislead you. I have seen many great meds being defamed as soon as they go generic.
Get ready for the big push to sell you new lutamides which are $12000 a month even if Extandi gives you seizures.Why Johnson & Johnson was fighting till last day in New Jersey court to keep Zytiga patented if Zytiga was bad...Now it is bad..because they can't rob patients families as it sells for about $1200 a month in US, about $400 a month in Europe and $100 a month in India. Time for profiteers to scare people and make them buy shamelessly expensive new meds.
Some patients and their doctors like Xtandi because there’s no requirement to take daily steroids. However, my father has a seizure while on Xtandi. I urge caution. Finally there’s a relatively simple genetic test that will save a patient a lot of time re: Zytiga.
I'm sorry, here it is: a blood test can determine if a biomarker, AR-V7 is present. This can help determine if abiraterone will work for the patient vs. taxane chemotherapy.
"Not all mCRPC patients respond to androgen receptor (AR)-targeted therapies, like abiraterone and enzalutamide.1 When AR-targeted therapy fails, acquired resistance could be the cause. The only predictive and prognostic test for men with mCRPC, the AR-V7 Nucleus Detect test:
Accurately identifies patients who will not benefit from AR-targeted therapies.
Is predictive of improved overall survival with taxanes versus AR-targeted therapies.
Provides easy-to-interpret results (a positive or negative result)."
This is from MALECARE. ADNA is a new blood test that will tell you if ZYTIGA and XTANDI will or will not treat CRPC. The AR-V7 test will determine that. I got my test processed at John Hopkins Lab and there is a west coast lab doing the blood test. Unfortunately I had problems getting the blood sample off using their special cold shipping container and the yellow specific vials. Medical centers here wouldn't process it for me so I had to do the dog work. Cost is $1000 and it is suppose to covered by Medicare. I received a bill but fought it. I could write a book on my experiences being here in a rural part of the country, but its done. A big medical center would do the work for you. I'm undetectable and on Zytiga,Lupron
My husbands PSA only went up on Zytiga. It doubled in 4 months from 10.01 in January 2018 to 30.87 in July 2018. So, in his case, that's probably true. He also did Provenge in January and February at the same time, so neither treatment worked. The only treatment that has lowered his PSA since his initial Lupron lowering has been the Lut-177. Still 4 months out from last treatment and he is still undetectable.
I don't think that Zytiga caused the cancer to grow more aggressively in my husband. I think that, when Zytiga stopped working, the cancer began to spread again as a natural progression in prostate cancer. Of course we never know do we?
Dad was on zytiga for a year ,had to stop because of side effects . I have been on Xtandi now for almost 36 months and not having anything I can’t live with 🤪🤪 My Doctor did say that I have been on Xtandi longer than most of his patients .
Hmmm. I'm castrate resistant with bone mets, on lupron post radiation, and now on Zytiga/prednisone. My PSA has been a roller coaster since nadir of zero in March 2019, 5 in October, now down to 1 after a month on Zytiga. Just got test results showing I do have an AR-V7 genetic variation in the tumor cores from my 2018 biopsy, the medic noted it and suggested there were additional blood tests. So I'm very interested in learning more.
I can only speak for myself, but Zytiga worked well for a year then psa started up as with everything. Slowly at first but rate picked up with each month. Side effects were minimal. Now on Xtandi, wow! Diarrhea big time for a couple months that’s slower now, but the low back pain is hard to get through. I’ve had two back operations years ago so I know pain. PSA is coming down slowly, but coming down. Good luck!
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 (abiraterone acetate)
Zytiga vs. Xtandi vs. Radium 223 vs. Cannabis
Zytiga vs Xtandi 
Enzalutamide or abiraterone
RT with ADT Relogolix (Orgovyx) vs Enzalutamide (Xtandi) Side Effect Differences?
