Preparing for Round Two

Hi, I am new to this forum. I was diagnosed with aggressive PCA in May, 2013 with a PSA of just below 1700 and a Gleason 8. The cancer had metastasized to my bones. My urologist put me on Zoladex (goserelin) and a bone strengthener Prolia (Denosumab). The effect was immediate and my PSA plummeted to undetectable. When it started to rise, my oncologist placed me on bi-calutamide and once again it went down to undetectable again. When it started to rise for a second time they took me off bi-calutamide and for the third time my PSA dropped. When it started to climb again, my oncologist switched me to Firmagon (degarelix). Although my PSA has gone from 1.3 in July to 2.4 in August (almost doubling) my testosterone level remains undetectable (less than 0.1).

I have appointments in September with my oncologist and two doctors at the Cancer Agency and I am guessing it won't be long before they put me on an androgen receptor inhibitory drug like Xtandi or Zytiga. My question is: "Is there a test to determine if I am susceptible to these drugs, prior to me taking them?"

23 Replies

  • In my personal experience, the oncologists and specialists I have seen in the USA have not considered genetic variations testing for possible efficacy before either Xtandi or Zytiga.

    There has been an "association" of an AR-V7 variation with lack of response, whether at first or after being on treatment for some time, but it may not be the only cause for either agent's not working, or ceasing to work fairly quickly, in a minority of cases.

    Here's a study from a few years ago that talks about it, in the research context.

    Here's a press release from a company that is hoping to sell their test, currently to researchers (only), to help them more tightly focus their future clinical trial / biological studies.

    In common clinical practice, I think the rapid PSA response (or not) (and/or rapid symptom relief) to either agent is typically used to decide if it is initially working.

    If you really want to seek a second opinion about it, you might consider contacting one of the principal authors of the research study listed above, e.g. In the USA, Dr. Emmanuel S. Antonarakis at Johns Hopkins.

    Just some thoughts and links,


  • Thanks so much Charles. Great information! Small world! See you at the PCRI Conference in September. Looks like it will be "Snuffy's Farewell".

  • When I first read your post, I thought you started treatment in May of this year, not 4 years ago. Must be my "chemo brain".

    It looks like you had a great response and got 4 years out of primary androgen deprivation therapy which is great. Normally that would mean that your prostate cancer is very "hormone sensitive" and will hopefully respond well to second line treatment such as Xtandi or Zytiga.

    If I was in your situation, I wouldn't do any additional testing unless second line ADT treatment didn't work. And you should know that fairly quickly.

    I'm not a doctor so you should ask yours.

    Good luck and keep us posted on your treatments and results.

    PS. How much time did you get out of Bicalutamide?

  • I appreciate your response. I think I will follow your advice and just wait and see. My pet peeve is doctors seem to give the same second line options (Enzalutamide and Zytiga) to all patients as if the cancer was homogenous when we know not all cancers are the same.

    To answer your question, the Casodex (bi-calutamide) along with Zoladex (goserelin) worked for about six months. When my PSA started rising again, my oncologist felt I was better off without it. As soon as I stopped taking Casodex my PSA went down.

  • I can see your concern. Prostate cancer is definitely not homogenous as you say, but your particular prostate cancer appears to be the type that is very responsive to androgen-based treatments. Those of us who aren't going to be cured are hoping that at least we can have a prostate cancer that stays androgen sensitive for as long as possible.

  • Thanks Gregg. I appreciate your response. I have been lucky so far (four years three months on ADT), but this is new territory for me.

  • So if PSA starts rising is stopping bicalutamide the first recommended action rather than jumping on Xtandi or Zytiga + prednisone? I've been on ADT3 off and on since September 2015.


  • Your PSA will often go down when you stop bicalutamide so that's usually the first step. It's called anti-androgen withdrawal. Here's an article about it.

  • Great link


  • Thank you kindly! I note that stopping the antiandrogen is not a therapeutic recommendation but it sure sounds like a good play if it can work for a goodly period. Most articles I've seen recommend staying on Lupron and adding Xtandi or Zytiga + .

    As usual there's no set formula for treating this lousy malady.


  • Typically, you stay on Lupron, but go off bicalutamide. Then when the PSA starts to rise again you add Zytiga plus prednisone or Xtandi but keep the Lupron going.

  • Gregg

    I like that idea. Just had PSA and t test today. Fingers crossed!



  • Thanks Gregg (and many others who replied to my initial post). I was told by my oncologist that Casodex (bi-calutamide) added to hormone therapy only works for a certain length of time. When your PSA starts to rise you are better off jettisoning Casodex and in many cases your PSA falls. That is what happened to me.

  • I think the cancer can eventually start to eat the Casodex. When it becomes food, that's when you have to take it away.

  • Thank you for the link.


  • I do not think the antiandrogen withdrawl response last that long, though one could also use a different antiandrogen like when Sartor switched me to Nilandron. at any rate for me I did not bother waiting for the 30% chance the cells became mutated and fed on I just continued with another therapy, today it is likely zytiga w steroid. But be careful because a small bump can often indicate noise i the labs or various other factor ie riding a bikebefore test. We are looking for at least 2 or 3 steady bumps. May be seen quiker with ultrasensitive psa,and the main object is to get as much time as we can out of each of these therapies, I am 11 plus years out dx2006stg4,bpsa148,GS10,widesprean metastatic disease to B and L , and suspicious lesion on lung, Lung later turned out to be just a 3cm shadow.

    all the best,


  • Be advised that on zytiga u will need to take the steroid prednisone. xtandi u don't need a steroid. Steroids have side effects

  • SIDN


  • I took zytiga for 4 years with only 5 mg prednisone, my expert said at the 5 mg dose , the body still produces some and keeps that ability,

  • Your body makes Cortisol, around the equivalent of 5-10mg of Prednisone per day. So when you take 10mg of Prednisone you are roughly doubling the amount your body makes.

  • Yes Gregg, and what My Expert told me was that if I just take 5 mg prednisone with zytiga, My body will still need to make Cortisol, and will retain that ability, this is why I was only on 5mg prednisone through about 4 years of zytiga.


  • Here was the perfect trial for you, but you missed it.

    Get to rub shoulders with people deep in the weeds of this.

  • Thanks Martin,

    I appreciate that medical researchers are at least investigating whether folks are going to respond to the second tier PCa drugs before they prescribe them. Thanks again for sharing.

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