My Story

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I am now, Dec 2016, age 81 years, married, in good health (apart from prostate cancer) height 178cm and weigh 85kg. I have moderately high blood pressure and  moderately high cholesterol  - both stable and controlled within normal range.

I am semi-retired and for the past eleven years my wife and I have been touring around Australia. We have a Mitsubishi Triton 4WD with a slide-on camper, plus a small Millard caravan. My hobbies are fishing and camping. I also spend heaps of time on my laptop computer and browsing the Internet.


Timeline of my prostate related events, with commentary:-

Oct 2000.  My local doctor in Deception Bay, Qld suggested during my regular yearly medical check, that I should have a PSA (blood test for prostate specific antigen) test. The result was that I had a PSA of 5.5ug/L (up to 4.00 was then regarded as not requiring further investigation, biopsy etc.).

The doctor did a per rectum digital (gloved finger) feel of my prostate (this procedure is also called a digital rectal examination, DRE). The gland felt normal and slightly enlarged. I was advised to have regular tests to see if there was any increase in the PSA level. Fourteen months later in December 2001 my PSA and DRE were unchanged.

Dec 2001. My PSA tests and DRE showed no change since October 2000.


Sept 2003. PSA 7.0ug/L.  I had become a bit lax in getting PSA checks done at regular intervals whilst I was touring and fishing around southern Queensland.  I was then given a referral to see a urologist, but as I was moving to NSW at that time I did not get to consult a urologist until November 2003.


Oct 2003.. PSA 10.23ug/L Free 35%, following a short course of antibiotic. I was now getting a little concerned. This result was not from my usual pathology lab and I have since discounted the result, because subsequent tests done by my usual lab over the next few months returned lower PSA results.

Nov 2003. I consulted a senior urologist at Lismore, NSW. He advised me to have a biopsy and said he could do the biopsy in his surgery immediately. I was given an antibiotic injection, asked to undress and get into a gown. About fifteen minutes later I was undergoing the procedure - a trans rectal ultra sound (TRUS) guided sextant biopsy. I was told the procedure would involve placing a TRUS device into the rectum and associated biopsy gun - a slender device equipped with a thin spring loaded needle that penetrates the rectum wall into the prostate and obtains a core specimen. Six cores were obtained, I felt a few clunks as the core samples were taken - no pain - and the whole thing was pretty much a non-event for me, but I am aware that others have found the procedure painful and embarrassing. I was given some antibiotic tablets to take for a few days and as expected, I had some blood in my urine and faeces.
A few days later I received a phone call from the urologist to advise me that one of the cores was positive for cancer. I was not surprised by the news, because I was aware from the rising PSA velocity over the past couple of years that cancer was a real possibility.
He asked me to see him at his surgery where he would discuss the pathological results and arrange for a abdomen/pelvic CAT scan and a whole body bone scan to be done. At his surgery he explained to me that one core of the right apex was five percent positive for cancer and the Gleason score was 3 + 3 = 6. Gleason grade is from 1 to 5 where 1 means the cancer cells closely resembles the prostatic tissue, have uniform patterns and within well defined boundaries. Gleason grades 4 and 5 indicate a more aggressive cancer because the cancer cells no longer look like prostate tissue, have random patterns with poorly defined boundaries. Gleason score should not be confused with Gleason grade. A Gleason score of 4 + 3 = 7 indicates that there is a pattern predominance of grade 4 cells followed by a second most common pattern of grade 3 cells.
The subsequent scans, as expected for such a localised cancer, showed no evidence of spread outside the prostate. The TNM stage was therefore T1cN0M0. The prostate volume was 78cc - enlarged.

TNM rating is a system for staging prostate cancer. T describes the extent of the primary cancer. T1c means that the tumour was identified by a biopsy done because of rising PSA. The N describes whether or not there has been any spread to nearby lymph nodes and M denotes whether or not there is metastasis or distant spread.
In other words I had a low volume, low to intermediate risk prostate cancer with no evidence of spread outside the prostate (localised). This diagnosis, even from day one, has never caused me any anxiety or loss of sleep. Perhaps I was relieved because I didn't have a high risk tumour.

Now, what was I to do?

The urologist said that I had treatment options to consider which included surgery, radiation and watchful waiting, The latter I prefer to call active surveillance or objective management. The objective being to move to interventional therapy, if and when the cancer progresses to a stage where I should do so. It seems that some low risk prostate cancers are in fact indolent, and are not likely to be a real issue re the average live expectancy of a 70 year old.

There is an excellent slide presentation re active surveillance is here.

The quandary is - which prostate cancers are likely to become aggressive and life threatening or remain slow growing and perhaps indolent?

The urologist gave me some literature to read and advised me that as there was no urgency, I should do some research and perhaps seek opinions from others before coming to a decision. In the literature I received was a copy of an article which appeared in Fortune magazine. The story, "Taking On Prostate Cancer" relates to Andy Grove (then CEO of Intel) and how he ultimately chose a therapy option when he was diagnosed with prostate cancer. There is a link to the article on the 'links' page.

My next step was to see what information I could find on the Internet. Because of the wealth of information available, I became engrossed and interested in research so much that it has become somewhat of a passion.


Jan 2004. PSA 7.7ug/L


Jan 2004. I consulted a leading senior radiation oncologist (Dr F) in Brisbane. He said he would accept me for radiation therapy. He also said he would require me to have a short course (3 months) of the anti-androgen hormone Zoladex (goserelin acetate)  to shrink the prostate. However, when I questioned him about the radiation therapy proposed and the equipment to be used, it quickly became apparent that better facilities were available in Sydney or Melbourne where 3D-CRT facilities existed. I knew IMRT (Intensity-Modulated  Radiation Therapy) was at that time commonly in use for prostate cancer in the U.S.A., but it seemed from my enquiries it was only available in Melbourne for selected patients - more about radiation therapy here. I decided against having radiation in Brisbane.  


Feb 2004. Whilst searching of the Internet, I found the prostate pointers website (see link on my links page) and joined the associated mailing list P2P (physician to patient). I posted my medical data on the mailing list. A reply of about 2 or 3 pages long came from Dr Stephen Strum, a USA medical oncologist with many years experience, since 1983 specialising in prostate cancer. He has authored or co-authored many books and research papers. I found the information he provided very helpful. He suggested that I take Avodart (dutasteride) and Cardura (doxazosin), but I strongly advise that before taking any medication, herbal medications or the like, you should as I did, get the OK from your physician. Doxazosin is unavailable in Australia and I import a generic brand. To interpret an isolated PSA value in a man treated with dutasteride, it is advised to double the actual PSA test result, if dutasteride has been taken for six months or more. (see dutasteride Articles 1   2  )

Feb 2004.  PSA 8.02ug/L, Free 14%.


Mar 2004. I consulted a senior medical oncologist (Dr B) at Tamworth Base Hospital, NSW. He is a visiting specialist to Tamworth from the Prince of Wales Hospital, Randwick, Sydney NSW. His comment was that I probably had low risk PCa and most men in my age group had a few cancer cells in their prostate. Advice - active surveillance.


Mar 2004. I consulted a senior radiation oncologist (Dr S) at Tamworth Base Hospital, NSW. He is a visiting specialist to Tamworth from the Prince of Wales Hospital, Randwick, Sydney NSW. His comment was that I probably had low/intermediate risk PCA. Advice - active surveillance, but radiation OK if that was my choice.


Apr 2004. Commenced doxazosin 4mg daily.


Jul 2004. Commenced dutasteride 0.5mg daily.

Feb 2005. PSA down to 3.0ug/L.  Prostate volume 41ml (was 82mls 11 May, 04) - big reduction due to dutasteride and doxazosin?


Feb 2005.  I consulted a radiation oncologist (Dr. F.)  at the Peter MacCallum Cancer Centre (PeterMac) in Melbourne and this was followed by an MRI with spectroscopy.  Report:- "Combination of MRI and MRS suggest that the site of dominant disease is within the mid to upper portion of the peripheral zone of the prostate gland posteriorly - multi focal small volume disease favoured. Findings correspond with Stage II disease. No features suggest extracapsular extension. The prostate gland volume is enlarged, measuring 41ml.  Gross benign prostatic hypertrophy (BPH) is demonstrated, compressing the peripheral zone."

I was offered 3D-CRT radiotherapy but I decide to continue on active surveillance. Besides, if I was to have radiation, I preferred to wait (if prudent) until IMRT became available for patients like me.

Since the dates when I commenced taking dutasteride and doxazosin, I have added some dietary supplements, vitamins and minerals, which may or may not be helpful. These are daily - pomegranate juice 200ml, Robert's Soy Compound - a couple of tablespoons on wheat biscuits for breakfast, vitamin E (succinate) chewable tablet, vitamin D3 and several cups of green tea. I also have a glass of tomato juice occasionally.
During the course of my motorhoming in Qld, NSW and Victoria I have had the opportunity to consult several senior specialists, which included four radiation oncologists, one medical oncologist and four urologists. Mainly, the specialists did an examination and the usual DRE and medical assessment re my suitability for their therapy. I was usually told the options available to me and it was for me to decide, but all have said that active surveillance was a reasonable course for me to take.

Dec 2006. MRI prostate and spectroscopy done at  Specialist Magnetic Resonance Imaging  (SMRI) in Sydney. Gland Volume 56ml (previously 41ml Feb 2005) - otherwise no significant change from the previous MRI-S study done Feb 2005 - no evidence of extracapsular extension.


OCT 2007.  Per rectum (DRE) prostate examination indicates the prostate is firm, smooth and moderately enlarged.


Nov, 2007.  MRI study (no spectroscopy) was done at Peter MacCallum Cancer Centre Melbourne. Prostate volume 66ml with a broad region of signal abnormality involving posterior aspect of superior prostate, presumably representing the known prostate adenocarcinoma. No evidence of extracapsular extension, seminal vesicle invasion or lymphadenopathy.

Jan 2008 PSA was total 2.0ug/L, free 0.7ug/L 33% (steady reduction since Feb17, 04 - then 8.02ug/L).

In my case PSA test results have to be discounted because I take dutasteride.

 May 2008. PSA 1.8ug/L - free 0.6, 36%.


Sept 2008. Per rectum (DRE) examination shows a soft, slightly enlarged prostate with no palpable nodules.

Sept 2008. I commenced bicalutamide with a view to reducing prostate and cancer volume, because radiation (IMRT) is on my short list of preferred options.  I am also very interested in the da Vinci robotic prostatectomy and this might be the way I shall go.

Sept 2008. PSA 0.32ug/L - free 0.1, 31%. (Low PSA due to the strong effect of the bicalutamide.)


Oct 18, 2008. Because of side effects of bicalutamide - breast soreness and breast tissue growth, I commenced Tamoxifen 10mg daily. I found this action to be very effective - soreness disappeared completely and also the hard tissue within the breasts cleared up completely - no further breast enlargement, but this was only minor. See article.


Nov 2008. MRI-S at SMRI; Gland volume 61ml, down from 66ml (Nov 07)  - no evidence of extra-capsular extension or seminal vesicle invasion. There is nodular enlargement of the central gland consistent with benign prostatic hypertrophy and the peripheral gland is attenuated. The spectroscopy demonstrated regions of elevated choline to citrate ratio within the central gland. Note: The prostate normally has a  high citrate to choline ratio and the reverse applies to prostate cancer. (See Abstract)


Jan 2009. Reduced Tamoxifen to 20mg weekly (Sunday). This was because of this article, which suggests 20mg once a week is sufficient.


Feb 2009.  I am curious as to whether or not the histology of the PCa has changed since the confirmed diagnosis in Nov, 2003. I could get another biopsy done, but I am reluctant to do so simply to satisfy my curiosity. No specialist has been able to provide me with evidence that a biopsy is incapable of spreading the cancer cells within or out of the prostate. There is an interesting article about MRI-S, biopsy and needle-tracking here


Feb 2009.  Stopped taking the bicalutamide and Tamoxifen. I have no problems with the combination (except the expense), but when I started I saw it as only a short course for a few months, to reduce the prostate volume (this occurred) and perhaps reduce the PCa volume.


May 2009.  PSA 1.1ug/L - free 0.3, 27% - strong effect of the bicalutamide.


Oct 2009. MRI with contrast was done on a latest model Tesla 3 machine, by Qld X-Ray at Coorparoo in Brisbane. Prostate volume now 71cc, down from 78cc when first diagnosed in 2003. Comment by radiologist, " Indication is either low volume or relatively indolent disease and there is no evidence of extracapsular extension of tumour. Comparing these appearances with the patient's previous MRI study performed in December '06 shows no significant interval change."


May 2010. Renal ultrasound to assess kidneys - all OK - prostate volume 73cc.


June 2010. Ceased doxazosin which I imported and switched to locally available prazosin (Minipress). Doxazosin and prazosin are both alpha-blockers that relax blood vessels and also the muscles surrounding the urethra. Because I have high blood pressure and moderate enlargement of the prostate (BPH) this drug is of benefit to me.


July 2010. PSA 2.3ug/L - free 0.8ug/L 35%. Also, my doctor did a per rectum (DRE) feel of my prostate and said it felt normal and only slightly enlarged.


Oct 2011. PSA 2.51ug/L - free 0.7ug/L 28%


May 2012. PSA 2.7ug/L - free 0.8ug/L 30%. Per rectum (DRE), prostate firm in apex area. No significant lumps or bumps felt.

May 2012. MRI (with contrast) at Wesley Medical Imaging (Wesley Hospital) Brisbane. The Wesley has up to date equipment & methodology, and claims that overseas data shows that 3T multiparametric prostate MRI (Which the Wesley uses) can detect clinically significant prostate cancer with an accuracy of 90%.

My MRI summary: No definitively abnormal areas. A patchy area of reduced T2 signal is noted right apex - possibly lower grade tumour. Note: This correlates to the original biopsy Nov 2003 which indicated 5% of core right apex was positive PCa.  Prostate volume 64ml so still down on 78ml as at Nov 2003. I guess that Avodart has had a large part to play in reducing the prostate volume.


Feb 2013. PSA 3.00ug/L - free 0.8ug/L 27% Note: PSA is increasing slowly. Effect of Avodart means that the PSA should be doubled for clinical assessment, i.e. 6.00ug/L, which is still lower than the 7.00ug/L in Sept 2003.


July 2013. Now age 77, I am feeling in good health and continue motorhoming - currently at Cairns. At the time of my diagnosis in 2003, and with a moderately/rapid rising PSA, I had reason to be concerned. As I approach 10 years from the diagnosis, I am happy with the path of active surveillance and the medications I have taken. If need be, I still have the option of radiation - perhaps even surgery.


April 2015. I should have updated My Story before this, but due to an email today asking me how I am, and reminding me that my last entry was back in 2013, I am back! I still continue with active surveillance, regular six monthly per rectum (DRE) prostate examinations and a PSA test every few months. I am happy to report that the DRE's find no real change, no lumps or bumps, prostate enlarged and firm with BPH evident. My last PSA test was done 23 Dec, 2014 and read 2.00 ug/L which is very good. However, I am still taking Avodart, which has a reducing effect on PSA, but most likely not affecting the cancer.  


Oct 2016. PSA 2.7 ug/L - same as May 2012.


To be continued.


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