43 with stage 4 prostate cancer

[Cam]

Hi Team,

 

My prostate cancer journey continues to be anything but ordinary: had blood test results today and my testosterone has actually risen from 1.1 to 1.7 following the orchiectomy 5 weeks ago. My GU Oncologist said he has never seen it before but says I’m not mCRPC because we have never achieved castration levels of testosterone.

 

Testorone rise has unfortunately fueled a rise in PSA from 0.034 to 0.248. Looking at cutting out all vitamins and supplements, and seeing a hormone therapist.... then regrouping.

 

Are we (and my Onc) just kidding ourselves and should we just accept that this is an indication that I’ve moved to castration resistance? Would welcome any opinions.

 

Cam

[Admin]

Far be it from me to challenge your MO, but at least by this definition:

• Castrate-resistant pca (crpc) is defined by disease progression despite androgen-deprivation therapy (adt) and may present as one or any combination of a continuous rise in serum levels of prostate-specific antigen (psa), progression of pre-existing disease, or appearance of new metastases.

does not need the actual achievement of castrate levels.

Ref: Hotte, 2010:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935714/

 

[Cam]

Thanks Jim,

 

In an endeavour to maintain some sanity and get a few hours sleep tonight, I’ll go with the optimistic side and use Hotte’s 2.2.1 ”Castrate-resistant pca is usually suspected in patients with new symptoms on adt, with a rising psa, or with new evidence of disease on bone scans or computed tomography scans. To determine the castrate-resistant state and to properly assign a clinical state, it is imperative that patients have a testosterone level drawn. If patients are non-castrate, androgen ablation therapy should be instituted or maximized. If patients have testosterone levels in the castrate range, the diagnosis of crpc can be made.

[stevecavill]

Given you have actually been castrated, seems odd to say you aren’t castrate resistant !  Testosterone is also made outside the testes.   Have you looked at an anti androgen such as bicalutamide ? That blocks the androgen receptors on the prostate cells. 

 

1.7 is still pretty low, you probably need another test in a few weeks to check the trajectory of the psa.  I cant recall from previous posts.  Have you had a PSMA scan to look for metastases?

Steve 

[Maffy]

Dear Cam,

 

I really feel your frustrations and your pain. I can wish you well but I know it does nothing. I can even say my thoughts are with you but that would be a lie and even my thoughts does nothing to comfort. The only thing can truly offer is my prayers for you and your family at this time. I know that my God, the God of the Bible, can heal and can comfort.

 

Blessings

 

Maffy

[Charles (Chuck) Maack]

Dear Cam,

 

The level 1.7 if nmol/L is equivalent to 50ng/dl, and 50ng/dl used to be considered castrate level but no longer so.  20ng/dl (0.68nmol/L) is the level considered castration level that has been achieved with androgen deprivation medications to reduce the testosterone level of active testicular/Leydig Cell production. With bilateral orchiectomy, testosterone, on average, falls to 15 ng/dL (0.5 nmol/L).  Using the explanation as to androgen (testosterone) produced from other sources, your orchiectomy has not sufficiently lowered testosterone to suppress PSA elevation.  An antiandrogen such as bicalutamide/generic of Casodex might suppress adrenal gland produced androgen from accessing cancer cell androgen receptors (AR).  Adding dutasteride/Avodart, a 5Alpha Reductase (5AR) inhibitor prescribed to inhibit androgen/testosterone from conversion to the stronger stimulant to cancer cell growth, dihydrotestosterone/DHT, might serve to inhibit any androgen not suppressed by the antiandrogen while enroute to 5AR and bring PSA down and manageable.  If these are not found effective, then either abiraterone/Zytiga to totally shut down testosterone production from all sources (testicular, adrenal glands, and that produced within cancer cells) or enzalutamide/Xtandi to block androgen access to cancer cell androgen receptors, may be alternatives – since these last two are extremely expensive medications, it would be important that they are covered under your government or private health insurance plan.  Please note that I am only expressing considerations to discuss with your treating physician (Medical Oncologist?). 

 

Testosterone from other sources than testicular:

 

Despite testicular shut down of testosterone production either by LHRH agonists/GnRH antagonist, the adrenal glands still secretes precursors to androgens such as testosterone and advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. (MY NOTE: Though the below reference goes into detail as to how androgen can be produced from other sources (adrenal glands, and cancer cells can produce androgen within themselves which, I believe, is derived from cholesterol) to fuel androgen “independent” cancer cells, the same can occur to continue to fuel androgen “dependent” cancer cells.)

 

FROM:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802176/ (I have emphasized in bold lettering that of interest)

 

"Results and Discussion

The results described in this study show for the first time that androgen-independent human prostate cancer cells are able to acquire complete steroidogenic potential and are capable of synthesizing testosterone from cholesterol, indicating an intracrine regulation of AR in advanced stages of prostate cancer. Several studies have shown the expression of key steroidogenic enzymes in prostate cancer cells indicating that these cells are able to synthesize androgens from adrenal precursors (El-Alfy, et. al., 1999,Nakamura, et. al., 2005,Stanbrough, et. al., 2006). The presence of functional AR in advanced stages of the disease and the presence of testosterone and DHT, sufficient to activate the AR, in cancer tissues under androgen ablation therapy, also support this notion (Gelmann, 2002,Mohler, et. al., 2004,Titus, et. al., 2005). The purpose of our studies was to determine whether prostate cancer cells in advanced stages of the disease can synthesize testosterone from cholesterol hence making them completely independent of serum testosterone and/or adrenal steroid precursors.

 

In conclusion, our results clearly show for the first time that advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. Our results also explain the essential role of AR in survival and proliferation of androgen- independent prostate cancers under androgen-ablation therapy and suggest that inhibitors of steroid biosynthesis in prostate cancer cells may be required to completely abolish the androgens in these tumors for its therapy."

 

 

DISCLAIMER: Please recognize that I am not a Medical Doctor.  Rather, I do consider myself a medical detective. I have been an avid student researching and studying prostate cancer as a survivor and continuing patient since 1992. I have dedicated my retirement years to continued deep research and study in order to serve as an advocate for prostate cancer awareness, and, from an activist patient’s viewpoint, as a mentor to voluntarily help patients, caregivers, and others interested develop an understanding of this insidious men’s disease, its treatment options, and the treatment of the side effects that often accompany treatment.  There is absolutely no charge for my mentoring – I provide this free service as one who has been there and hoping to make their journey one with better understanding and knowledge than was available to me when I was diagnosed so many years ago.  IMPORTANTLY, readers of medical information I may provide are provided this “disclaimer” to make certain they understand that the comments or recommendations I make are not intended to be the procedure to blindly follow; rather, they are to be reviewed as MY OPINION, then used for further personal research, study, and subsequent discussion with the medical professional/physician providing their prostate cancer care.

 

Charles (Chuck) Maack - Prostate Cancer Patient/Activist/Mentor

(A mentor should be someone who offers courtesy, professionalism, respect, wisdom, knowledge, and support to help you achieve your goals; would that I succeed) Website: www.theprostateadvocate.com 

 

[Cam]

1 hour ago, Charles (Chuck) Maack said:

Dear Cam,

 

The level 1.7 if nmol/L is equivalent to 50ng/dl, and 50ng/dl used to be considered castrate level but no longer so.  20ng/dl (0.68nmol/L) is the level considered castration level that has been achieved with androgen deprivation medications to reduce the testosterone level of active testicular/Leydig Cell production. With bilateral orchiectomy, testosterone, on average, falls to 15 ng/dL (0.5 nmol/L).  Using the explanation as to androgen (testosterone) produced from other sources, your orchiectomy has not sufficiently lowered testosterone to suppress PSA elevation.  An antiandrogen such as bicalutamide/generic of Casodex might suppress adrenal gland produced androgen from accessing cancer cell androgen receptors (AR).  Adding dutasteride/Avodart, a 5Alpha Reductase (5AR) inhibitor prescribed to inhibit androgen/testosterone from conversion to the stronger stimulant to cancer cell growth, dihydrotestosterone/DHT, might serve to inhibit any androgen not suppressed by the antiandrogen while enroute to 5AR and bring PSA down and manageable.  If these are not found effective, then either abiraterone/Zytiga to totally shut down testosterone production from all sources (testicular, adrenal glands, and that produced within cancer cells) or enzalutamide/Xtandi to block androgen access to cancer cell androgen receptors, may be alternatives – since these last two are extremely expensive medications, it would be important that they are covered under your government or private health insurance plan.  Please note that I am only expressing considerations to discuss with your treating physician (Medical Oncologist?). 

 

Testosterone from other sources than testicular:

 

Despite testicular shut down of testosterone production either by LHRH agonists/GnRH antagonist, the adrenal glands still secretes precursors to androgens such as testosterone and advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. (MY NOTE: Though the below reference goes into detail as to how androgen can be produced from other sources (adrenal glands, and cancer cells can produce androgen within themselves which, I believe, is derived from cholesterol) to fuel androgen “independent” cancer cells, the same can occur to continue to fuel androgen “dependent” cancer cells.)

 

FROM:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802176/ (I have emphasized in bold lettering that of interest)

 

"Results and Discussion

The results described in this study show for the first time that androgen-independent human prostate cancer cells are able to acquire complete steroidogenic potential and are capable of synthesizing testosterone from cholesterol, indicating an intracrine regulation of AR in advanced stages of prostate cancer. Several studies have shown the expression of key steroidogenic enzymes in prostate cancer cells indicating that these cells are able to synthesize androgens from adrenal precursors (El-Alfy, et. al., 1999,Nakamura, et. al., 2005,Stanbrough, et. al., 2006). The presence of functional AR in advanced stages of the disease and the presence of testosterone and DHT, sufficient to activate the AR, in cancer tissues under androgen ablation therapy, also support this notion (Gelmann, 2002,Mohler, et. al., 2004,Titus, et. al., 2005). The purpose of our studies was to determine whether prostate cancer cells in advanced stages of the disease can synthesize testosterone from cholesterol hence making them completely independent of serum testosterone and/or adrenal steroid precursors.

 

In conclusion, our results clearly show for the first time that advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. Our results also explain the essential role of AR in survival and proliferation of androgen- independent prostate cancers under androgen-ablation therapy and suggest that inhibitors of steroid biosynthesis in prostate cancer cells may be required to completely abolish the androgens in these tumors for its therapy."

 

 

DISCLAIMER: Please recognize that I am not a Medical Doctor.  Rather, I do consider myself a medical detective. I have been an avid student researching and studying prostate cancer as a survivor and continuing patient since 1992. I have dedicated my retirement years to continued deep research and study in order to serve as an advocate for prostate cancer awareness, and, from an activist patient’s viewpoint, as a mentor to voluntarily help patients, caregivers, and others interested develop an understanding of this insidious men’s disease, its treatment options, and the treatment of the side effects that often accompany treatment.  There is absolutely no charge for my mentoring – I provide this free service as one who has been there and hoping to make their journey one with better understanding and knowledge than was available to me when I was diagnosed so many years ago.  IMPORTANTLY, readers of medical information I may provide are provided this “disclaimer” to make certain they understand that the comments or recommendations I make are not intended to be the procedure to blindly follow; rather, they are to be reviewed as MY OPINION, then used for further personal research, study, and subsequent discussion with the medical professional/physician providing their prostate cancer care.

 

Charles (Chuck) Maack - Prostate Cancer Patient/Activist/Mentor

(A mentor should be someone who offers courtesy, professionalism, respect, wisdom, knowledge, and support to help you achieve your goals; would that I succeed) Website: www.theprostateadvocate.com 

 

Thanks Chuck, just 15 months into this nightmare and following a robotic RP, ADT, multiple mop up surgeries, 6 rounds of docetaxel, 3 rounds of SBRT, and a bilateral orchiectomy..... I was just hoping for some good news for once (seems that's not coming).  I will digest you valuable information and discuss with my Oncologist.  Cam.

[Barree]

Hi Cam,

Chuck has really summed up all the relevant information very concisely and the might helps are in my opinion certainly very worthy of consideration and discussion with your MO.

Just a couple of points – Casodex when initially taken can on occasions cause a spike in PSA levels rather than a reduction - so if and when you commencing taking Casodex  it is necessary to monitor your PSA regularly and often.

The other consideration relates to Avodart ( Dutasteride). When you  take Avodart  and other 5-ARIs after 6–12 months of treatment they can reduce serum PSA levels by up to 50%, even if cancer is still present at the existing  level. . It is important to measure serum PSA levels  6–12 months after starting Avodart or combination treatment - to establish a new PSA baseline (Nadir).

After 6 months on Avodart  to compare treatment levels with normal (untreated) ranges, for comparison purposes it is necessary to multiply the measured serum PSA value by 2.

[Cam]

11 minutes ago, Barree said:

Hi Cam,

 

Chuck has really summed up all the relevant information very concisely and the might helps are in my opinion certainly very worthy of consideration and discussion with your MO.

 

Just a couple of points – Casodex when initially taken can on occasions cause a spike in PSA levels rather than a reduction - so if and when you commencing taking Casodex  it is necessary to monitor your PSA regularly and often.

 

The other consideration relates to Avodart ( Dutasteride). When you  take Avodart  and other 5-ARIs after 6–12 months of treatment they can reduce serum PSA levels by up to 50%, even if cancer is still present at the existing  level. . It is important to measure serum PSA levels  6–12 months after starting Avodart or combination treatment - to establish a new PSA baseline (Nadir).

 

After 6 months on Avodart  to compare treatment levels with normal (untreated) ranges, for comparison purposes it is necessary to multiply the measured serum PSA value by 2.

 

Plenty to digest as usual, feedback is so very much appreciated.

[Cam]

Hi all, the advanced PCa roller coaster continues and I'm overdue to share an update.  Following the unexplained testosterone and PSA rise 5 weeks post bilateral orchiectomy, I did as the MO suggested and cut out all supplements.  I was also following a relatively strict Keto diet that I started late May (initially for weight loss rather than PCa reasons) and still am.  My next set of blood test results on July 2 had PSA down to 0.076 and testosterone at 0.9..... another anxious few weeks then August 21 results had PSA at 0.033 with T at 0.6 (the number we were aiming for after undergoing the orchiectomy).  Latest results on October 2 had PSA at 0.020 at T still at 0.6.

 

I'm mentally shot from the stress of all the uncertainty and the fact that I feel that we aren't doing anything now other than waiting for a PSA rise.  Since diagnosis in Jan 2017 we've been aggressively attacking the cancel with RP, ADT, Docetaxel, SBRT and finally the orchiectomy on April 30 this year, but now I'm on no medication and are feeling quite lost.  I suppose I should just focus on life, but that's easier said than done when I know there is cancer still inside me.  I'd rather be actively attacking the cancer whilst classified as mHSPC but it seems I've exhausted the available "proven" treatments and should be saving newer treatments for later.  The acceptance of the inevitability of progressing to mCRPC is something I struggle to deal with.

 

Cam

[Cam]

Latest news: 21 months since diagnosis and only a couple of weeks away from my 45th birthday, it appears my cancer may have become mCRPC.  Numbers are low with rises from 0.02 to 0.043 to 0.072 in a 7 week period, but depression and stress levels are very high.  Really hoped that the RP, ADT, docetaxel, SBRT and ultimate orchiectomy would buy me more time before having to wade my way through the castrate resistant nightmare of options.  

 

Oh well, meeting medonc this afternoon for what will certainly be another enjoyable conversation.

Cam

[pauldhodson]

Hi Cam, Sorry to hear it. This happened to me 12 months ago. I'm still here, so try not to lose hope. The next big break through might be just around the corner. Cheers Paul.

[Cam]

1 hour ago, pauldhodson said:

Hi Cam, Sorry to hear it. This happened to me 12 months ago. I'm still here, so try not to lose hope. The next big break through might be just around the corner. Cheers Paul.

Thanks Paul.  We could certainly do with a breakthrough!!

[alanbarlee]

G'day Cam,

While you're considering the next round of treatment options with your medonc / radonc team, you might want to look at having a chat with a psycho-oncologist. This is a specialty area of support which could bring you relief from the stress, anxiety and depression that is clearly hitting you hard at this stage of your journey, as it does with so many men - especially younger men.

I have a friend in Melbourne who works in this area, who has guided me over the years: I strongly recommend such a referral.

Best wishes,

Alan 

 

 

[Cam]

6 hours ago, alanbarlee said:

G'day Cam,

While you're considering the next round of treatment options with your medonc / radonc team, you might want to look at having a chat with a psycho-oncologist. This is a specialty area of support which could bring you relief from the stress, anxiety and depression that is clearly hitting you hard at this stage of your journey, as it does with so many men - especially younger men.

I have a friend in Melbourne who works in this area, who has guided me over the years: I strongly recommend such a referral.

Best wishes,

Alan 

 

 

 

 

Sounds like a good idea Alan! Saw MO yesterday and the news wasn’t good. Put the hard word on as to his guesstimate of life exptancy based on the bad histopathology and the findings in the comprehensive cancer panel... and the fact that my cancer has progressed quickly in spite of us throwing the kitchen sink at it... and it looks like I’m here for a good time, not a long time. Started bicalutamide and have a PSMA PET/CT in a week. Going to try to enjoy a European vacation dec 11- Jan 14 then I’m assuming I’ll be put on Abiraterone and hope it lasts more than a few months.

 

Won’t be accepting defeat just as I need to see my boys grow up and the youngest just turned 5.... but the battle is wearing me down.

Cam

 

[Maffy]

On 10/10/2018 at 12:26 PM, Cam said:

Hi all, the advanced PCa roller coaster continues and I'm overdue to share an update.  Following the unexplained testosterone and PSA rise 5 weeks post bilateral orchiectomy, I did as the MO suggested and cut out all supplements.  I was also following a relatively strict Keto diet that I started late May (initially for weight loss rather than PCa reasons) and still am.  My next set of blood test results on July 2 had PSA down to 0.076 and testosterone at 0.9..... another anxious few weeks then August 21 results had PSA at 0.033 with T at 0.6 (the number we were aiming for after undergoing the orchiectomy).  Latest results on October 2 had PSA at 0.020 at T still at 0.6.

 

I'm mentally shot from the stress of all the uncertainty and the fact that I feel that we aren't doing anything now other than waiting for a PSA rise.  Since diagnosis in Jan 2017 we've been aggressively attacking the cancel with RP, ADT, Docetaxel, SBRT and finally the orchiectomy on April 30 this year, but now I'm on no medication and are feeling quite lost.  I suppose I should just focus on life, but that's easier said than done when I know there is cancer still inside me.  I'd rather be actively attacking the cancer whilst classified as mHSPC but it seems I've exhausted the available "proven" treatments and should be saving newer treatments for later.  The acceptance of the inevitability of progressing to mCRPC is something I struggle to deal with.

 

Cam

Dear Cam,

 

I'll keep you in my prayers. Mine was like yours - very low PSA for about 3 years before it was discovered that a rare type of PCa was raging. Anyway, I'm going on to 24 months after RP (on the 21st of Nov) and 12 months after Chemo+ADT, still on ADT; next assessment on Dec 12 (always stressful times) but hopeful - PSA is still undetectable thus far. Not sure when the ADT will be off; my Onco said to keep it going for the time being. Blessings Maffy.

[pauldhodson]

9 hours ago, Cam said:

 

 

Sounds like a good idea Alan! Saw MO yesterday and the news wasn’t good. Put the hard word on as to his guesstimate of life exptancy based on the bad histopathology and the findings in the comprehensive cancer panel... and the fact that my cancer has progressed quickly in spite of us throwing the kitchen sink at it... and it looks like I’m here for a good time, not a long time. Started bicalutamide and have a PSMA PET/CT in a week. Going to try to enjoy a European vacation dec 11- Jan 14 then I’m assuming I’ll be put on Abiraterone and hope it lasts more than a few months.

 

Won’t be accepting defeat just as I need to see my boys grow up and the youngest just turned 5.... but the battle is wearing me down.

Cam

 

 

Try not to 'own' that life expectancy BS, they haven't go a clue. I think the mind is a powerful thing, you will become what you believe. Trust me, I know it's hard not to go to that dark place. I chatted with a guy on Facebook recently given 6 months and he's 11 years past his use by date!

[Cam]

5 hours ago, Maffy said:

Dear Cam,

 

I'll keep you in my prayers. Mine was like yours - very low PSA for about 3 years before it was discovered that a rare type of PCa was raging. Anyway, I'm going on to 24 months after RP (on the 21st of Nov) and 12 months after Chemo+ADT, still on ADT; next assessment on Dec 12 (always stressful times) but hopeful - PSA is still undetectable thus far. Not sure when the ADT will be off; my Onco said to keep it going for the time being. Blessings Maffy.

Thanks Maffy!  Hope you continue to keep the cancer in check.

[Cam]

2 hours ago, pauldhodson said:

 

Try not to 'own' that life expectancy BS, they haven't go a clue. I think the mind is a powerful thing, you will become what you believe. Trust me, I know it's hard not to go to that dark place. I chatted with a guy on Facebook recently given 6 months and he's 11 years past his use by date!

 

Good advice Paul.  I've fallen into a deep dark hole, but I will dig myself out.

[Cam]

Hi fellow members, does anyway have any experience with Provenge?  I’ve been on bicalutamide since my PSA rises in Nov ‘18 following bilateral orchiectomy (and a host of other treatments since Gleason 9 diagnosis in Jan ‘17) but are considering other options given small PSA rises again (from 0.073 when I started bicalutamide, down to 0.054 in Feb, up to 0.057 in March and today 0.067.... testosterone at lowest point 0.4).  Saw MO today and again raised Provenge.  He said he wouldn’t do it, but said I should consider it if money isn’t an issue (which it isn’t as the only issue to me is staying around long enough to see my 5, 7 & 10yo boys grow into adults).  The information regarding Provenge is a bit of a mixed bag and my biggest issue is actually co-ordinating treatments if I have to have them in the US.  Is it worth the effort at 45yo or should I just continue on bicalutamide until PSA rises further then look at Enzalutamide or Abiraterone as suggested by my MO?  As always, any advice/thoughts/opinions are very much appreciated.  I’m in LA/San Francisco from May 1 to 9 and will try to see someone in the US for another opinion re: Provenge.

 

I’m not good at sitting back and waiting for the PSA to rise so I’d much rather be attacking the cancer.

Cheers,

Cam

[alanbarlee]

G'day Cam,

If it were me, with a significant serial increase in PSA from your very low current levels, I'd be taking your MO's advice and promptly moving off bicalutamide (Cosudex) and across to either abiraterone (Zytiga - a T-synthesis inhibitor which has been great for me ) or enzalutamide (which is several times more potent an anti-androgen than bicalutamide). Both of these have very manageable side effect profiles and both are subsidised on the PBS.

 

Another possibility to pursue with your doc could be adding dutasteride (Avodart), which inhibits enzymic conversion of T (and yours isn't quite as low as one might like) to DHT, which is several times more active a fuel for PCa than T. It also seems to help Zytiga do its job a bit better, as does low-dose dexamethasone.

 

If you want to spend a bit of money in the USA, rather than spending it on Provenge (which you can't get in Oz, and which seems to give only small improvements in mean overall survival), you might do worse than lining up some gene testing there instead, which may provide a roadmap for future treatment if you happen to have one or more suspect mutations - either germline (inherited) or somatic (in the tumours - possibly treatment-induced). There are a few commercial panels available: you should seek advice from your medonc as to which might be the best one for you.

 

Keep in mind that there are continuing immunotherapy trials going on with combinations of PD-1 / PD-L1 /  CTLA-4  inhibitors like pembrolizumab, nivolumab and ipilimumab. Although for most patients PCa isn't succumbing to these drugs as dramatically as melanoma, there is some expectation that the researchers will find a way. Check with your medonc.

 

Best wishes,

 

Alan

[Cam]

7 hours ago, alanbarlee said:

G'day Cam,

If it were me, with a significant serial increase in PSA from your very low current levels, I'd be taking your MO's advice and promptly moving off bicalutamide (Cosudex) and across to either abiraterone (Zytiga - a T-synthesis inhibitor which has been great for me ) or enzalutamide (which is several times more potent an anti-androgen than bicalutamide). Both of these have very manageable side effect profiles and both are subsidised on the PBS.

 

Another possibility to pursue with your doc could be adding dutasteride (Avodart), which inhibits enzymic conversion of T (and yours isn't quite as low as one might like) to DHT, which is several times more active a fuel for PCa than T. It also seems to help Zytiga do its job a bit better, as does low-dose dexamethasone.

 

If you want to spend a bit of money in the USA, rather than spending it on Provenge (which you can't get in Oz, and which seems to give only small improvements in mean overall survival), you might do worse than lining up some gene testing there instead, which may provide a roadmap for future treatment if you happen to have one or more suspect mutations - either germline (inherited) or somatic (in the tumours - possibly treatment-induced). There are a few commercial panels available: you should seek advice from your medonc as to which might be the best one for you.

 

Keep in mind that there are continuing immunotherapy trials going on with combinations of PD-1 / PD-L1 /  CTLA-4  inhibitors like pembrolizumab, nivolumab and ipilimumab. Although for most patients PCa isn't succumbing to these drugs as dramatically as melanoma, there is some expectation that the researchers will find a way. Check with your medonc.

 

Best wishes,

 

Alan

 

Hi Alan, you always reply and I really appreciate your suggestions. 

 

I’ve been on Finasteride 1mg for many years (initially the vanity of hair loss) but all MO’s have told me to stick with it.

 

I had a Comprehensive Cancer Panel done on original tumor at PeterMac last June and the summary was:

- No somatic mutations detected
- TMPRSS2-ERG gene fusion detected consistent with prostate carcinoma diagnosis
• PTEN, FAS loss of heterozygosity detected with prognostic significance. IHC confirmation recommended.

 

When presented to my MO, he said there was nothing “actionable” in the report. He has no plans for me to do further testing and I did raise it again yesterday.

 

He would rather me stick to bicalutamide until a more substantial PSA rise is detected, but I struggle with the “wait for it to kill you” approach.  I’ve been told to accept that the cancer will kill me, but I’d prefer to go out fighting rather than laying down my sword. I figure the longer I keep it in check and have some sort of quality of life with my wife and boys, the more chance a curative solution may appear.... hence the Provenge investigation which appears to only add a few months to OS... but they may be the important months in the future.

 

Best wishes to you too Alan.

Cam

[Charles (Chuck) Maack]

Dear Cam,

 

This paper provides a pretty good picture of the current medications used in patients with your status, including whether or not Provenge/sipuleucel-T is merited. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5131740/. When you look at the time frame involved in its administration – at least 4 weeks on site– and cost – last I was aware somewhere in the vicinity of $93,000 U.S. (not to mention what would be your cost in travel and accommodations during that period) – this becomes a very considerable expense that has shown only short extension of life if successful. I tend to agree with Alan as to what should be your best options locally to bring under better control and management your current status.  From what you mention of your current treating physician, it appears he/she is NOT up to par on appropriate treatment for patients with your status.  To encourage you merely remain on bicalutamide/generic of Casodex is, in my opinion, not medically sound. If approved and available in Australia, and more importantly is covered by your health insurance, either enzalutamide/Xtandi or abiraterone/Zytiga should be your next step.  These two, also, are otherwise very expensive medications.  The reference provided herein explains what each contribute to appropriate treatment, and certainly are in order.  Alan also suggests their consideration, as do I.  I also am a strong proponent of the medication dutasteride/Avodart in androgen deprivation treatment to inhibit T conversion to the more powerful stimulant to PCa growth and proliferation dihydrotestosterone/DHT; preferred over finasteride/Proscar since finasteride only inhibits Type II 5Alpha-Redutase (5AR) isoenzymes, wherein dutasteride inhibits both Type II and Type I, and Type I is found to increase in advanced PCa.  I also recommend that you have your Prolactin level determined; this importance is explained here: https://tinyurl.com/7w5omeo.  I see it important that you need to find a physician in your locality with much more expertise in the treatment of advance prostate cancer than the physician currently overseeing your condition.  Perhaps some of your mates in Australis can chime in with their knowledge of such physicians in your locality.

Charles (Chuck) Maack (ECaP) - Continuing Prostate Cancer Patient Since 1992, Advocate, Activist, Volunteer Mentor since 1996 to men diagnosed with Prostate Cancer and their Caregivers locally and on-line Worldwide. www.theprostateadvocate.com

[Charles (Chuck) Maack]

I see it important to add: 

PLEASE NOTE: Medications involved in Androgen Deprivation Therapy (ADT) are known to increase cardiovascular risk.  Thus, IT IS IMPORTANT that prior to prescribing any form of ADT medication the patient’s other health issues, that would include already present cardiovascular issues, are determined.  As noted in:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516188/ 

 

“Androgen deprivation therapy (ADT) has been the mainstay of treatment for advanced prostate cancer for decades, and has been shown to control disease and improve symptoms. In addition, for men with high-risk localized or locally advanced prostate cancer, short-course ADT in combination with radiotherapy improves survival. There is evidence that ADT increases cardiovascular risk, particularly in men with preexisting cardiovascular disease. This increased risk may apply even with short-course ADT. In an individual patient, the benefits of ADT should be balanced against the risk, and patients who require ADT should have risk factors for cardiovascular disease optimized. There is some evidence to suggest that more contemporary methods of delivering ADT may reduce cardiovascular risk.”

 

Dr. Matthew Roe, a Professor of Medicine at Duke University’s Clinical Research Institute (DCRI), the Faculty Director of the Global Outcomes Commercial MegaTrials program, and the Director of their Fellowship Program, remarks: “If a patient who has advanced prostate cancer and known cardiovascular disease is being considered for androgen deprivation therapy, it is important that he speak with his cardiologist. (Presumably, both a cardiologist or cardiovascular specialist and an urologist or oncologist would treat him.) He needs to ensure that all the providers have a discussion about what the best and safest treatment would be before therapy begins. Obviously, this trial (the PRONOUNCE trial regarding which is safer for patients with cardiovascular issues, the GnRH agonist Lupron or antagonist Firmagon (or neither?) https://tinyurl.com/yxnw5kb6 ) is not completed yet so we don’t have any answers. In the meantime, it is certainly in the patient’s best interest to ensure that his providers are communicating and trying to jointly determine the right approach.”

[Cam]

Thanks for the very useful information Chuck.  It's so frustrating to have PSA at 0.067 (after the plethora of treatments I've endured) and not be able to cure this horrible disease.  I'm sure I'm not the only one, but accepting that this cancer is going to eventually defeat me as there's no cure, is almost impossible to come to terms with.

 

Cheers,

Cam