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Tony Max - My prostate cancer journey

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tonymax

by tonymax » August 16th, 2011, 11:28 am

Born 1946,lived Sydney northern beaches during childhood.

Obtained science and economics degrees in 1966 and 1973.

Worked in paint industry for 40 years – mostly at Taubmans at Villawood.

Career covered technical,sales,marketing,production,logistics areas.

I retired from work in 2006 age 60.

Married Robyn in 1977 – 4 children and 5 grandchildren (so far).

Lived at Carlingford 1977-99 and Dural last 10 years.

Interests included 16 foot skiff sailing on Sydney Harbour,some social golf

and more recently a project on the distribution of native plants in SE Australia.

Diagnosed with prostate cancer (PSA 6,Gleason 8) in 2003 – radical that year.

Everything was clean and looked good but PSA did not drop so spread had occurred.

All scans were clear so location could not be found.

Have been on continuous hormone treatment (Lucrin) since Oct 2003.

PSA dropped to low of 0.07 and then rose doubling every 6 months.

By Feb 2010 PSA was 6.7 so started Cosudex with continuing Lucrin.

Further CT scans were then done and were still clear – so no radiation options.

One week after Cosudex start PSA had dropped to 5.6 so looks like it is going down.

Next PSA test in a week or two so fingers crossed.

Vitamin D/calcium/some Zometa are maintaining good bone density.

Contacted one of the prostate cancer organizations in 2003 and they put me on to Max Gardner.

Had 2 or 3 extended phone sessions with Max and he helped me tremendously – settled me down,lots of relevant info and basically gave me a roadmap for the path ahead – the sort of things Support Groups are good at.

My radical was done at Westmead and as this was halfway between work and home

I joined the Westmead Support Group in 2003 and have attended most of their meetings since then.

I also occasionally attend other groups eg the San,North Shore and St Vincents in the early days.

Recently attended the Charles Myers lecture at the Garvan and the Joe Enis talk at North Shore – very interested in their approaches to treatment of advanced prostate cancer versus the more conventional methods – will probably make my medical oncologist’s life a misery with plenty of questions on the differences.

While we depend on the technical expertise of the doctors as prostate cancer patients we have to manage our own illness as well and the support groups can help greatly in this.

UPDATE March 2011

Background

1.My gut feel is that any treatments will be more successful the smaller the cancer.Given the exponential growth pattern of cancer minimising the size for as long as possible is desirable.

2.I understand that I am now approaching a stage where there is no “official” treatment and waiting to allow the development of bone mets to justify the use of chemotherapy may be the usual course. In my opinion this is not the right way to go if any other options are available.

3.I wish to delay the use of chemotherapy for as long as possible. While access to new drugs may be facilitated by taking chemo earlier I am concerned that the chemo treatment may close off some attractive options later.

4.Cancer is an individual disease so being proactive and trying a variety of treatments (in a controlled way) gives the best chance of finding one that may benefit me. I want to be proactive.

5.My finances are modest and leaving my wife in a state of penury from my health costs is not an option. However judicious use of some money to break through MBS/PBS roadblocks is a possibility.

6.Some anti cancer options may increase risks of heart attack or stroke. My blood pressure and cholesterol levels have been well controlled for many years so I would be prepared to tolerate some increased risk of heart attack or stroke where the risk from the cancer appears the greater.

7.”Indolent” Gleason 8 cancer, continuing Lucrin since Oct 2003, Cosudex 50mg since Feb 2010 (PSA dropped from 6 in Feb 2010 to 2.8 in Aug 2010 and risen to 3.9 Feb 2011). Daily medications are Pravachol 40mg for cholesterol, Micardis 200mg for blood pressure, Celebrex 40mg, Vitamin D3 2000 IU, Caltrate 600mg and Cosudex above. Most days I also have about 150ml pomegranate juice. Most pathology tests seem pretty good but hovering a bit closer to diabetes so this will need to be watched. Bone density now normal – 3 bisphosphonate infusions approx 2004-2005. CT scan in 2010 still clean.

Options

1.Low dose Aspirin helps with heart attacks and recent surveys have confirmed some benefits against prostate cancer. Benefits may well be minor but no dramas in taking it so nothing to lose. Suggested dose 75-100mg per day perhaps the slow acting version to eliminate stomach irritation. Would propose to start this immediately.

2.Moving from low dose Cosudex (50mg) to high dose – no great benefits as far as I am aware and side effects will increase – although current side effects on 50mg are quite manageable.

3.Going off Cosudex apparently gives a short temporary lowering of PSA but this is very much temporary.

4.Increasing Celebrex above current low dose. This is based on the possibility of Celebrex or the Celebrex/Pravachol combination having some anti cancer capability. This is yet to be shown in live humans – a Phase 3 trial on the Celebrex/Pravachol combo is under way but still has a fair way to run. I have been on this combination since Oct 2003 so maybe it is contributing to my “indolence” – or maybe it is not. Increasing Celebrex may increase risk of heart attack.

5.Triple blockade by adding dutasteride (Avodart) to my current treatment may be worth a try to buy some more time. Understand this tends to be used on less aggressive cancers and it artificially lowers PSA results (perhaps halved?). My Gleason 8 is “indolent” so I may get some benefit and discussions with some local and overseas people did not negate this possibility – I am tending towards this as the next step.

6.Second line hormone therapy based on Ketoconazole and additional drugs (Leukine/Oestrogen Patches – Myers or Hydrocortisone – Sholz). This option allegedly gives extended benefit to many people but it is tricky and laborious to administer and control and side effects can be a problem. Leukine is very expensive as well. If this option is available it may be worth consideration a little further down the track.

7.New hormone treatment drugs Abiraterone,MDV3100 and others are in the pipeline but still some way off. Abiraterone has completed post-chemo phase 3 trial very successfully and phase 3 pre-chemo trial under way. Side effects are claimed to be negligible.Availability on PBS and timing for that questionable given latest Roxon announcement. MDV3100 and others further behind. Trying to hang out for availability of these is the main battle for me as I see it. Snuffy Myers told me in Chicago that he has patients doing well on Ketoconazole who did not respond to Abiraterone – guess cancer is an individual thing and trying a variety of options is desirable.

8.Now the wildcard – talked to a guy in the advocacy side who has advanced PCa – had PET scan which discovered hotspot (invisible to CT) central front of body half way between prostate and chin. He had external beam radiation which appears to have knocked it – repeat PET clean and negligible PSA for some time now. He must be in the know – got first PET free and second for $800. Mine of course may not be in one place – may be all over the place by now. Radiation oncologist at Westmead was wary about possible dangers of EBR too far away from the prostate bed but EBR operators at Macquarie Uni Private Hospital did not seem too concerned – maybe their gear is better than Westmead. My repeat CT at Westmead last year was clean but if I could get myself a PET scan it might be worth it.

UPDATE Tuesday, 16 August 2011

Added Avodart to Lucrin and Cosudex Mar 2011 with PSA at 3.9 (up from 2.8 6 months before which was Cosudex nadir).

Next PSA test later this week + bone density + diabetes checks.

My oncologist is running MDV3100 trial but would need metastases identified by CT or bone scan (not MRI or PET) to qualify for that so I will probably not be eligible.

He is also running abiraterone trial (without those conditions) so I will probably be eligible for that.

So depending on what my PSA is doing I will need to make some decisions shortly.

UPDATE Tuesday 21 Feb 21 2012

PSA at 18/8/11 was 5.7 so the Avodart is no use.

Avodart and Cosudex discontinued to see if the removal of the Cosudex gives a benefit.

Bone density results were slight lessening in spine area (back to mild osteopenia) but hip still fine.

Doctors not concerned at spine bone density at this stage.

PSA on 5/12/11 has increased to 10 - removal of Cosudex giving no benefit.

Decision made to add Anandron 150mg daily (Nilutamide - secondary hormone treatment) to the ongoing Lucrin.

Repeat CT and bone scans done - both still clean.

My pushing to get PET scans done were previously unsuccessful so now I tried lobbying for MRI - with similar unsuccessful results.

I had been hovering on the edge of diabetes for some time but after further tests now officially have the disease - few symptoms yet - need to look at diet and exercise again.

Started taking Diabex 2x500mg daily (Metformin) early Dec as well - for the diabetes.

Doctors indicated it might help a bit with the cancer.

PSA on 10/2/12 has increased to 11.

Looks like the Nilutamide might be holding it a bit, somewhat reduced rate of increase.

Next PSA test to be done mid April.

My doctor has a new proposal - a new type of PET scan is about to become available in a public hospital nearby.

He will try to get me this PET scan in the next couple of weeks.

If this shows up cancer then a CT scan could be heavily focussed on that area and may also show the cancer.

If it does I would be eligible for the pre chemo PREVAIL MDV3100 trial that may finish recruiting mid 2012.

This is a real game of poker - watch this space.

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Admin

Tony

Something to perhaps think about and talk about with your doctors:

Dr Snuffy Myers says that leaving Taxotere too late makes often makes the patient too ill for other treatment.

His video is summarized here:

Taxotere before too ill

or

http://advancedprostatecanceraustralia.ipbhost.com/index.php?/topic/260-ask-dr-snuffy-myers-video-taxotere-early-rather-than-late/

The video is found at:

http://askdrmyers.wordpress.com/2011/08/10/starting-taxotere-for-pca/

Jim

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Admin

Tony

With PSA rising and no cancer spots found, have you considered an MRI of the axial spine?

If metastases are found early, and are small in number, burning them out with focused radiotherapy has been found to be successful.

Click on this link to read an abstract describing how MRI of the axial spine is more successful than other scanning methods:

http://advancedprostatecanceraustralia.ipbhost.com/index.php?/topic/392-encore-mri-of-spine-best-identifier-of-metastases/

Cheers

Jim

Edited by Admin
Link was to old forum

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Admin

Tony

My interpretation of the paper mentioned above (IANAD):

Standard sequential work-up (SW) = standard practice:

bs = standard bone scan (an X-ray that is taken (often a few on the same day at different times) after you have been injected with a tracer (technetium-99m))

txr = targeted x-rays

MRI = x-ray like images made with magnetism

MRIor = MRI on request.

MRIas = MRI of the axial spine

In short the usual practice if you suspect metastasis:

You do a bone scan. (BS)

Anything not clear but suspicious - take X-rays of the part. (TXR)

Anything not clear but suspicious after the bone scan + X-ray (BS/TXR) - do an MRI.

This was compared with just starting with an axial MRI of your spine. (MRIax) (Axial just means direction the pictures are taken in. Bascially parallel to the soles of your feet)

The key result was:

Sensitivities were:

46% for BS alone,

63% for BS/TXR,

83% for BS/TXR/MRIor, and

100% for MRIas; (So an MRI correctly identified all people with metastases, while a bone scan alone missed 54% of them).

The corresponding specificities were 32%, 64%, 100%, and 88%, respectively. (So the MRI incorrectly identifies 12% of people without metastases as having metastases).

The very important result:

MRIas identified metastases in seven (30%) of 23 patients considered negative and eight (47%) of 17 patients considered equivocal by other strategies, which altered the initially planned therapy.

i.e. Starting with MRI by itself identified metastases that were missed by other strategies.

Hope this is a little clearer.

(Remember: I am not a doctor.)

Cheers

Jim

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JimJimJimJim

Tony

Your belief that Celebrex helped is boosted by this article from Beyond the Abstract

Note it is only a lab study on human prostate cancer cells in mice.

Regression of prostate tumors upon combination of hormone ablation therapy and Celecoxib in vivo, by Per Borgström, PhD, et al.

Fri, 01 July 2011

BERKELEY, CA (UroToday.com) - Advanced prostate cancer is normally treated by hormone therapy, i.e. withdrawal of androgens.

This treatment controls tumor growth at first, however invariably results in the development of androgen-dependent tumors and relapse. Improving the effectiveness of hormone therapy and delaying relapse is crucial, as 40,000 men still die of prostate cancer every year in the US.

Epidemiological studies have shown beneficial, potentially protective effects of anti-inflammatory COX-2 inhibitors such as FDA-approved Celecoxib (Celebrex) in various types of cancer. In addition, knock-out of the COX-2 gene in mice decreases tumor formation, whereas COX-2 overexpression promotes cancer progression. Clinical trials have demonstrated the safety of Celecoxib, but so far have shown few clinical benefits for the treatment of prostate cancer in various therapeutic settings. However, the drug has not been tested at the time of androgen therapy, despite a study showing that it suppressed the re-growth of LNCaP xenografts following androgen withdrawal.

To address this issue, we tested the efficacy of combining androgen withdrawal with Celecoxib, and we examined the respective physiological effects of Celecoxib and androgen withdrawal in vivo. To this end, we used IntraVital Microscopy (IVM) in a mouse model of prostate cancer.

IVM is used to visualize tumors in animals and analyze various aspects of cancer physiology such as tumor growth/regression, tumor vascularization, and cell migration. The main advantages of IVM include the real-time analysis of dynamic processes with single-cell resolution. Importantly, IVM offers the possibility to follow tumor growth/regression in a non-invasive, non-destructive manner. Since the application of IVM is limited to animal models that bear visually accessible tumors, we used the dorsal skinfold chamber model, in which a titanium frame with a viewing window is placed in the skin fold of the back of a mouse.

Mouse prostate tissue is grafted in the chamber and the graft develops its own vasculature and serves as orthotopic stroma for the tumor. This method emerged from early experiments showing that various syngeneic tissues grafted in rodent dorsal chambers do re-vascularize and survive over long periods of time. A small number of prostate cancer cells (TRAMP-C2 cells derived from a TRAMP mouse) are implanted on top of the prostate stroma. Indeed, it is now well known that the tumor microenvironment is crucial for the progression of almost every type of cancer, and that orthotopic implantation of cancer cells recapitulate human disease much more closely than subcutaneous implantation. Tumors grow faster and develop less leaky vasculature when the cancer cells are implanted into the relevant organ. Thus, co-implanting mouse prostate cancer cells with prostate stroma provides the tumor cells with an environment that better reflects the clinical disease compared to purely subcutaneous models. Importantly, re-vascularized stromal tissue and implanted tumors remain viable for long periods of time (up to 90 days).

Our laboratory uses tumor cells transfected with histone H2B-GFP fusion protein, which is incorporated into the chromatin without affecting cell cycle progression. Tumor cell fluorescence allows one to measure angiogenic activity, tumor cell migration, and parameters pertaining to tumor growth or regression such as mitosis, apoptosis and cell cycle arrest, all in the context of the host. The number of cancer cells in a growing tumor can be determined accurately from the fluorescence intensity by using a calibration curve. H2B-GFP makes it very simple to visualize metaphase-telophase DNA and apoptotic/pyknotic nuclei using high magnification images, and to calculate the number of cells undergoing mitosis or apoptosis. Finally, vascular parameters (vascular area, vascular length; average tumor vessel diameter and vascular density) are analyzed from video recordings using a photodensitometric computer software.

Thus, we co-implanted mouse prostate tumor cells with prostate tissue and allowed it to re-vascularize. Treatment was initiated once the prostate tissue and implanted tumors were established and vascularized. Celecoxib was administered twice daily (15mg/kg). Hormone therapy was administered in the form of surgical castration or chemical ablation, alone or in combination with Celecoxib. Four treatment groups were studied: control, untreated non-castrated mice; castration alone, Celecoxib alone, castration combined with Celecoxib.

Surgical or chemical castration inhibited angiogenesis and caused a disruption in the tumor vasculature which resulted in arrested tumor growth. The combination of androgen ablation with Celecoxib was synergistic, and was the only treatment to cause tumor regression through the combined effects of decreased angiogenesis, mitotic arrest and increased apoptosis of tumor cells. In vitro, Celecoxib inhibited the proliferation of prostate cancer cells mostly by inducing mitotic failure. In vivo, Celecoxib also caused mitotic arrest in the tumor cells and thus blocked tumor growth. Interestingly, the drug did not possess angiostatic activity.

In conclusion, the combination of hormone ablation with Celecoxib caused a profound regression of prostate tumors, and may delay progression toward androgen-independence in patients with advanced prostate cancer undergoing hormone therapy.

Written by:

Parisa Abedinpour, Véronique T. Baron, John Welsh and Per Borgström as part of Beyond the Abstract on UroToday.com. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc... of their research by referencing the published abstract.

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tonymax

Update 12/11/13

 

Sorry delay since last update - I have been slack.

I added Anandron (Nilutamide) to my ongoing Lucrin and started Metformin for my newly diagnosed Type 2 diabetes in Dec 2011.

My PSA results since are

18/8/2011     5.7

5/12/2011     10

10/2/2012     11

12/4/2012     10        Dihydrotestosterone level <0.5 (0.7-5.1)

24/7/2012     11        Testosterone level 0.2 (9.5-28.0)

25/8/2012     11         Bone density tests OK

10/11/2012   12

1/2/2013       12

2/8/2013       16

25/9/2013     16

5/11/2013     24

Nilutamide was discontinued early Aug 2013 following initial 16 PSA. 

PSA tests in Sep and Nov 2013 to qualify for Xtandi (Enzalutamide) clinical trials that require <10 months PSA doubling time.

Nov PSA result satisfies that requirement.

Type 2 diabetes seems under control and Metformin continues.

Lucrin primary hormone treatment continues.

 

So now some decisions are needed in the clinical trials maze.

The drug candidates are

Xtandi (Enzalutamide or MDV3100) from Astellas/Medivation

Zytiga (Abiraterone) from Janssen

ARN509 (Enzalutamide look alike) from Aragon

Alpharadin (Radium 223) from Algeta/Bayer

In Aug 2013 I was told about two trials coming up

Prosper involving Xtandi and Spartan involving ARN509.

Both required <10 months PSA doubling time and both have 2 arms - 2 parts active and 1 part placebo.

Today I have been told that Prosper starts next month and Spartan a little afterwards.

Also that I cannot switch from one to the other if I think I may be on placebo based on PSA non response.

Also that to qualify for either I must have clean standard CT and bone scans as measured just before the trial starts.

Also that if I wish to drop out of one of these trials due to non response I can do so and should then be eligible for a combined Alpharadin/Zytiga trial.

But wait it gets more exciting.

If my std CT/bone scans are not clean re prostate cancer I am eligible for an MDV3100-10 trial where every participant gets Xtandi (Enzalutamide) initially and when that benefit exhausts the trial is split into two halves - one half switches to Zytiga and the other half continues on a combination of Xtandi and Zytiga. This trial will commence early 2014. All participants get the active drug as it would not be ethical to put men with metastases on placebo.

All of the above is pre chemo - I have not had chemotherapy to date.

My CT and bone scans in 2003 were clean and a repeat CT scan in 2010 was also clean.

I still have no cancer symptoms, only the side effects from treatments.

So looks like my next decision is whether I have the CT/bone scans done in December, or January, (or later??).

Things are getting interesting.

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tonymax

Update 12/11/13

 

Sorry delay since last update - I have been slack.

I added Anandron (Nilutamide) to my ongoing Lucrin and started Metformin for my newly diagnosed Type 2 diabetes in Dec 2011.

My PSA results since are

18/8/2011     5.7

5/12/2011     10

10/2/2012     11

12/4/2012     10        Dihydrotestosterone level <0.5 (0.7-5.1)

24/7/2012     11        Testosterone level 0.2 (9.5-28.0)

25/8/2012     11         Bone density tests OK

10/11/2012   12

1/2/2013       12

2/8/2013       16

25/9/2013     16

5/11/2013     24

Nilutamide was discontinued early Aug 2013 following initial 16 PSA. 

PSA tests in Sep and Nov 2013 to qualify for Xtandi (Enzalutamide) clinical trials that require <10 months PSA doubling time.

Nov PSA result satisfies that requirement.

Type 2 diabetes seems under control and Metformin continues.

Lucrin primary hormone treatment continues.

 

So now some decisions are needed in the clinical trials maze.

The drug candidates are

Xtandi (Enzalutamide or MDV3100) from Astellas/Medivation

Zytiga (Abiraterone) from Janssen

ARN509 (Enzalutamide look alike) from Aragon

Alpharadin (Radium 223) from Algeta/Bayer

In Aug 2013 I was told about two trials coming up

Prosper involving Xtandi and Spartan involving ARN509.

Both required <10 months PSA doubling time and both have 2 arms - 2 parts active and 1 part placebo.

Today I have been told that Prosper starts next month and Spartan a little afterwards.

Also that I cannot switch from one to the other if I think I may be on placebo based on PSA non response.

Also that to qualify for either I must have clean standard CT and bone scans as measured just before the trial starts.

Also that if I wish to drop out of one of these trials due to non response I can do so and should then be eligible for a combined Alpharadin/Zytiga trial.

But wait it gets more exciting.

If my std CT/bone scans are not clean re prostate cancer I am eligible for an MDV3100-10 trial where every participant gets Xtandi (Enzalutamide) initially and when that benefit exhausts the trial is split into two halves - one half switches to Zytiga and the other half continues on a combination of Xtandi and Zytiga. This trial will commence early 2014. All participants get the active drug as it would not be ethical to put men with metastases on placebo.

All of the above is pre chemo - I have not had chemotherapy to date.

My CT and bone scans in 2003 were clean and a repeat CT scan in 2010 was also clean.

I still have no cancer symptoms, only the side effects from treatments.

So looks like my next decision is whether I have the CT/bone scans done in December, or January, (or later??).

Things are getting interesting.

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tonymax

Well I had the CT and Bone Scans done in Feb - plus a PSA of course.

The PSA had increased to 61 and we finally found the bugger on the CT scan after 11 years.

A 3.3 x 3.6 x 4.3 cm tumour in the right pelvic lymph node - the rest of the CT scan and the bone scan still clean.

My med oncol discussed with multi disciplinary team (MDT) and they suggested radiation.

However I now qualified for PLATO MDV3100-10 trial and given microscopic stuff probably in lots of places after 11 years I elected to go with that first and med oncol did not disagree.

Then it got more interesting.

Trial managers announced that Aust sites recruiting faster than overseas sites so they put a hold on recruiting here for 8 weeks to allow the others to catch up - I still stayed with PLATO and waited.

Another PSA early May - dropped back to 59!

So I no longer qualified for PLATO - PSA had to be rising.

So waited 3 more weeks to late May and rechecked PSA - 65.

PSA rising again and hold on recruiting now lifted so I finally got a guernsy on PLATO.

Next clinic to actually start the trial was 4/6 but I had an important meeting that day so delayed start to following clinic on 18/6.

As it turned out that pushed things past the limit but it did give me an extra marker - tumour pain.

For a fair bit of that last two weeks I had pain from the tumour most days - maybe 5/10 and controlled reasonably with the odd panadeine forte.

Went to clinic on 18/6 and got my first bottle of Enzalutamide tablets and started taking them.

Some pain still next day 19/6 but pain free all of the six days from 20/6 to now 25/6.

So this marker tells me something beneficial seems to be happening.

Next PSA in 3 weeks then 8 weeks after that (PSA also done on 18/6 but dont know result of that yet)

 

Updated 1 January 2015

 

With the trial we are doing two sequences of PSA tests to monitor results:

 

1.Local pathology lab (Douglass)

Results 65 (June 14), 38, 25, 15, 20 (end Nov) and 13 (23 Dec)

 

2.Official trial pathology lab in Singapore

Singapore result end Nov was 14.

 

It looks like my PSA results are bottoming out in the 10-15 range and the local end Nov result is incorrect.

 

What side effects have I had from my treatment so far on the trial?  My main side effect from Lucrin over the last 11-12 years has been fatigue – in my case always there but manageable.

The only side effect I get from Enzalutamide is substantially increased fatigue – to the point of needing a doze most afternoons.  Talking to doctors and patients, substantially increased fatigue is the main Enzalutamide side effect for most men.

 

I have a Clinical Trial consultation every 4 weeks and, of course, I chat with the other guys in the waiting room – and they with me. Their PSA’s at start of the trial vary a lot – 30 to 500 on the guys I have talked to.

All seem to be getting a reasonable response but the details vary a lot – how fast it drops, how low it goes, how long it stays there etc etc.

 

Watch this space

Tony M

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tonymax

Well guys I have been on Stage 1 of this pre chemo clinical trial (Xtandi =Enzalutamide) for 18 months now.

Based on my waiting room chats most fellows have derived benefit from the trial with substantial drops in PSA.

A proportion have already bottomed out, their PSA has begun to rise and they have been shifted to Stage 2 of the trial.

This is randomised to two arms - straight Zytiga (Abiraterone) or a mix of Zytiga and Xtandi.

In my last post I indicated I thought my PSA may be bottoming out at 10-15 range.

Well I was wrong, the good news for me is my PSA has still not bottomed - it continues to decrease.

My side effects are still manageable and I must admit I am falling in love with Enzalutamide.

My PSA results ex official trial Singapore lab are

18/6/14    69

19/9/14    21.8

3/12/14    14

29/12/14  10.4

28/1/15     9.3

25/2/15     8.72

25/3/15    10.03

22/4/15     7.33

20/5/15     7.26

17/6/15     6.45

15/7/15     5.95

12/8/15     5.00

9/9/15       5.20

7/10/15     4.24

4/11/15     3.90

2/12/15     2.70

30/12/15   Next test

 

I continue to take my full dose of Enzalutamide (4 tablets/day) and get my quarterly Lucrin shot.

I am extremely fortunate to be gaining max time benefit from the Enzalutamide with no end to that in sight yet.

When Enzalutamide was originally trialled on post chemo patients the average survival benefit was about 4 months.

Given my pre chemo status I currently have a survival benefit of 2 years plus - and maybe much more.

Given my results and my waiting room straw polls these new drugs should be available on PBS pre chemo.

Men are dying much earlier than they need to - we must break through the bureaucratic nightmare on this.

 

Tony Maxwell      6/12/15

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Charles (Chuck) Maack

Enzalutamide/Xtandi has been working very well for you, Tony.  I had similar dramatic effect in PSA drop when I started abiraterone/Zytiga some years ago.  I have generally managed my PSA level with close attention to levels and have moved from Zytiga to Xtandi then back to Zytiga and currently, since I have a good supply of both, I am taking two 250mg abiraterone "with dinner" daily along with two 40mg enzalutamide every-other day, along with dutasteride/Avodart 0,5mg on capsule every third day (just as effective as taken daily once established in one's system for at least 4 to 6 months), and continued Lupron every six months and Prolia also every six months.  I've been on/off Metformin (accompanied by Vitamin B12 since Metformin can deplete this important vitamin) but couldn't really tell if it was playing any role.  Since Metformin can also cause problems for some health issues (though good for others) I decided to just stop this medication.  My latest PSA was 2.07ng/ml and PSA levels previous were only over that twice and lower than that for many years; yet, if I went off these PSA/cancer cell managing medications my PSA would promptly start elevating.  More recently (just a few weeks ago) I learned of and had administered the radiotracer/isotope fluciclovine (Axumin) that when injected  travels directly to cancer cell activity and can be viewed with F18 PET/CT imaging.  AFTER ALL THESE YEARS ON ADT, this product settled on 1cm of activity near my anastomosis (connection of urethra to bladder neck) when, 26 years ago, I had my prostate gland surgically removed in "Open" surgery. The imaging was from top of my head down to mid thigh, and all was clear of any other presence of activity.  So, all this time it was never metastasized to bone.  It appears that with my research and study and appropriate prescribing of medications pretty much dictated by me, I have kept this location of cancer cell activity under control for the past 22 years on ADT.  Local CT, Body, and MRI imaging has never been sensitive enough to identify this location prior to my learning of this radiotracer recently obtained by the University of Kansas (USA) Medical Center nuclear 177 miles north of my home in Wichita, Kansas.  That imaging has now been meshed with another CT scan and MRI, and the MRI determined that the area may be slightly larger than 1cm and the activity slightly pushing at the side of my rectal wall.  I began "Targeted" radiation directly to the imaged location with what is known as EDGE radiotherapy just this past Thursday, and will have four more treatments with next Tuesday and Thursday and then the following Tuesday and Thursday.  I am ecstatic in the hope that finally my cancer just might be totally eradicated after 26 years since initially diagnosed!

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tonymax

Chuck,

 

Good to hear from you and thanks for all that info.

My ADT journey is now at the 15 year mark (Gleason 8) after failed radical in 2003 - age now 72.

Continuing Lupron and just over 4 years on Enza now.

Enza on a clinical trial - the only way I can access it affordably in Australia.

I cannot change my treatment regime and stay on the trial so am constrained in that sense.

My PSA continues just under or just over 1.0

Was put on (and remain on) Metformin for type 2 diabetes before starting Enza.

Am getting more benefit from Enza than most of the guys on the trial.

Some recent comments that Metformin may help to reactivate Enza - not sure about that.

My MO mentioned last visit that he has another patient still going strong on Enza after 8 years.

Will check to see if he is also on Metformin.

My pathology is very good although Vit B12 is a bit low - presume due to Metformin from your comments.

 

Only lesion in my pelvic lymph node - rest of body clean (CT and bone scans) after 15 years.

These scans pretty primitive but still hard to get more sophisticated ones in Aust.

I am amazed that the cancer may not have spread from the one location in 15 years!

My plan is when Enza starts to fail I consider perhaps some Abiraterone or some form of radiation to the lymph node.

In the meantime will stick with the Enza and clinical trial.

Good luck with your radiation treatment and please keep me posted on your progress.

Very happy to follow in your footsteps on this one.

 

Regards           Tony

 

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Charles (Chuck) Maack

I will be posting the results of my targeted radiation far and wide once the radiation is completed and can determine subsequent PSA level.  I would expect that if successful, and if cancer is not located anywhere else not having been identified in my specialized radiotracer/isotope imaging, my PSA should show up in ultrasensitive reading below 0.01ng/ml.  I pray that will be so! 

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tonymax

Still on Enza - 4 pills per day.

See attached data and graph.

May it long continue         Tony           Tony Max PSA Results.xlsx

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tonymax

Some relevant extra comments

1.My PLATO clinical trial has now expired but I continue to get the free Enza while I am deriving benefit from it. PSA checks now quarterly rather than monthly. Quarterly Lucrin shots continue.

2.Coincidentally I had a kidney stone back in 2014 and another one late 2017. The doctors for that did CT scans at the times and informed me in 2017 that my pelvic lymph node tumour was then only 12% of the size it was in 2014 - good stuff.

3.The response to Enza varies hugely - patient to patient. Only about 10% of patients match my experience so far. The need for multiple treatment      options is glaringly obvious to anybody - Russian Roulette on treatment access is criminal.

4.Fatigue still major side effect for me - worse than on Lucrin alone - but still manageable.

   Balance seems affected - no climbing high ladders or romping on roofs, suitable care re trip hazards

   Short term memory loss still an issue but not getting worse.

5.Evaluated by cardiologist recently - my heart seems fine. They have strengthened my blood pressure treatment tablets so BP 120/80 max         now versus 150-160/90-100 before.

6.My Type 2 diabetes puddles along with little change - Janumet 1000/50 seems to control it pretty well.

7.My general pathology and body chemistry all look pretty good.

8.When the Enza starts to fail I will consider radiation to the lymph node, particularly if rest of scans are clean.

 

I consider myself very lucky to be in this state after 15 years.

We simply have to expand this luck to more guys with access to new treatments at earlier stages of the disease.

 

Tony

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alanbarlee

Uplifting reports, Tony and Chuck!

 

At nearly 16 years, my experience is similar to yours. 

 

Following biopsy and a surprisingly unsuccessful open RP (PSA 5.6 / GS 7.5),  an 18FDG  PET/CT scan eventually confirmed prior micrometastatic escape, with a string of six pelvic and lower abdominal lymph nodes showing up as avid. Intermittent ADT3 treatment (Zoladex / Cosudex / Avodart) controlled PSA for several years, but the PCa eventually  became castrate resistant - but still no bone mets (with a NaF18 PET/CT scan). 5 1/2 years of pre-chemo Zytiga and 0.5 mg/day of dexamethasone, on top of continuing Zoladex and Avodart has produced a great result, with PSA holding at 0.02, i.e. only just detectable - likely arising from an (as yet) not quite dead met in one retroperineal lymph node. I'm close to claiming dormancy as per Snuffy Myers' criterion.

 

My only real issue has been sarcopenia, with loss of muscle mass in my quads and forearms - which I'm trying to stabilise with resistance exercise workouts in our local gym. I have no problem with bone density or weight, and lipids, glucose, liver enzymes and renal markers are all OK. 

Fatigue isn't a great problem, and occasional hot flashes are quite manageable. It's interesting that here we have 3 cases of very survivable lymph node mets, which the literature says usually are associated with a relatively poor prognosis. Second generation ADT seems to have moved the needle - a lot!

 

Best wishes,

 

Alan      

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tonymax

Chuck and Alan,

 

Had a meeting with Lisa Horvath in Sydney last Monday re her latest prostate cancer research project proposal.

I mentioned why dont researchers look at performance outliers in more depth to get potential clues on why they are so.

Guess this is what registries do but maybe there is more than one way to skin a cat.

She said Anthony Joshua at the Garvan in Sydney is putting such a program together.

Maybe we should volunteer our services

 

Tony

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alanbarlee

Very happy to be a guinea pig, Tony!

 

Alan

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