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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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