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John and Jane's Bumpy Road

John Murphy

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Introduction - if you wish
From being a healthy person all my life,succumbing to aggressive prostate cancer at 58 came as a huge shock to my system, lifestyle and business. I was also diagnosed with kidney cancer, which was cleared with a partial nephrectomy in 2006. I am happily married with 4 loving and supportive adult children and 7 grandchildren.

Month and year of diagnosis. Example: June 2009
Feb 2005

Age at diagnosis. Example 61 years

PSA at diagnosis. Example: 7.7

Gleason score at diagnosis. (from biopsy) Examples: 7 OR 3+4

Biopsy details. Examples: Positive cores 7/12 (58%) OR (R: 4+5 75%, 4+5 75%, 4+5 95%, 4+3 20%, 3+4 15% L: -, -, -, -, -, 3+4 50%) 
12 cores, 4 benign, 8 positive. 4+3=7. One core grade 5 making Gleason more like 8. 

Bone scan result at diagnosis. Examples: Clear OR Metastases in pelvis and lower spine
Bone scans 4th rib, possible sacrum and T7.

Lymph nodes at diagnosis. Examples: Clear OR CT scan shows 2 lymph nodes positive
CT's, negative lymph node involvement.

Capsular penetration (growth through prostate wall). Examples: None OR MRI shows probable extra capsular extension at left base in midline surrounding seminal vesicles and ejaculatory ducts
Some capsular extension.

Highest PSA before treatment. Example: 10.4

Initial treatment - surgery. Examples: Robotic prostatectomy OR open prostatectomy
No surgery.

Initial treatment - radiation. Examples: External beam OR brachytherapy OR HDR brachytherapy boost
No treatment to prostate.

Initial treatment - hormone therapy. Examples: Zoladex, continuous OR Zoladex + Cosudex intermittent after initial 12 months
Hormone therapy (Lucrin), for 12 months

Initial treatment - other. Examples: Immediate chemotherapy with Taxotere OR HIFU (High Intensity Focussed Ultrasound)

Lowest PSA after initial treatment. Example: 0.2

Testosterone after treatment. Examples: 6 nmol/L after 6 months, 15 nmol/L after 18 months
Testosterone 10.9 after 20 months.
Testosterone 3.3 after 5 years.
Testosterone 0.7 current

Month and year of recurrence. Example: June 2012
November 2006

PSA at recurrence. Example: 2.7

Testosterone at recurrence. Example: 0.5 nmol/L

Bone scan result at recurrence. Examples: Clear OR Metastases in pelvis and lower spine
Results are inconclusive but metastases still clearly present in 4th rib.

Other scan result at recurrence. Examples: CT scan clear OR Pelvic MRI with IV contrast shows recurrence in prostate bed
MRI shows obvious cancer in prostate bed. Not surprising as I still have a prostate.

Recurrence treatment - radiation. Example: External beam to prostate bed OR External beam to 2 bone metastases
External beam to my 4th rib. A course of 5 treatments, in 2006.

Recurrence treatment - hormone therapy. Examples: Zoladex + Cosudex continuous OR Nilutamide
Intermittent therapy for 18 months. After recurrence started triple hormone therapy for 13 months, as per Dr Leibovich, i.e. Lucrin,150 mg Cosudex and Proscar. I then took Prostasol for 2 years which kept my PSA low (<0.5).

Recurrence treatment - chemotherapy. Example: Taxotere, three weekly
Nil to date, however, maybe some Taxotere in the future. I hope I can avoid this.

Recurrence treatment - other. Example: On trial of Zytiga (abiraterone acetate)
Hoping to get on a Zytiga trial

Current treatment status. Examples: Continuing ADT OR Monitoring PSA each 6 weeks
Continuing ADT with PSA monitoring every 6 weeks.

Last few PSA scores with dates. Example: PSA 0.04 Jul 2011, PSA 0.05 Sep 2011, PSA 0.07 Feb 2012, PSA 0.11 Jul 2012
Latest PSA October 2013, 41

Final paragraphs - anything else you wish to say
I feel I am at a crossroad. My oncologist has held off with chemotherapy as my lifestyle and quality of life is still reasonable.
I am not quite sure whether to wait until I become really sick.
My eligibility for trials is limited as I still have not had treatment on my prostate.
I continue to enjoy life and work hard at the things that I think help. That is, I exercise regularly,including daily weights, my diet is healthy and I meditate daily as well.
I also follow Snuffy Myers' blog, which I find helpful.
My Vit D levels at time of diagnosis was < 50, now it is > 100.
My bone density levels are at this time good. 
Thank you for this opportunity to participate and thank you for the excellent forum. 

Date updated. Example 23 September 2012


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The mention by John that there was some Gleason 5. If that amounted to 5 percent of a core, the European Urological Assoc. protocol would replace the second number in the score, because of its considered significance.




I have extracted some of the text and made passing comments as in italics to save your reading the lot, but I do not deny you that right.



In needle biopsy, it is recommended that the worst grade always should be included, even if it is

present in < 5% of biopsy material (3).

current international convention, the (modified) Gleason score of cancers detected in a prostate

biopsy consists of the Gleason grade of the dominant (most extensive) carcinoma component plus

the highest grade, irrespective of its extent (no 5% rule).

 The presence of perineural invasion is usually reported, even though there is conflicting evidence

about its usefulness as a prognosticator of unfavourable disease  (42, 43). The proportion (%) or

length (mm) of tumour involvement per biopsy site correlates with tumour volume, extraprostatic

extension and prognosis after prostatectomy (43-45) and should therefore be recorded. The

length of carcinoma (mm) and the percentage of carcinoma involvement of the biopsy have equal

prognostic impact

International Society of Urological Pathology consensus recommendations for Gleason grading

was seen on the secondary pattern, which had the lowest percentage of concordance and was

reflected in a change toward higher Gleason prognostic groups. Of 172 patients in whom the

Gleason prognostic group was changed (to higher grades) based solely on the consensus criteria,

46 (26.7%) had a higher pre-operative PSA level, more extensive tumours and positive surgical

margins, and a higher pathological stage. In this series, the revised Gleason grading identified

more patients in the aggressive prognostic group Gleason score 8–10, who had a significantly

shorter time to biochemical progression-free outcome after radical prostatectomy


The primary extension assessment of prostate cancer (PCa) is usually made by digital rectal

examination (DRE), prostate-specific antigen (PSA) measurement and bone scan, supplemented

with computed tomography (CT) or magnetic resonance imaging (MRI) and chest X-ray in specific

situations. The Prostatic Acid Phosphatase (PAP) test seems to be forgotten in these "modern"

times. It has prognostic significance as found in fairly recent studies.

more extensive examinations for adequate T-staging are only recommended in selected cases

when more precise staging directly affects the treatment decision, i.e. when curative treatment is

an option . TNM staging is of all three elements. N&M may be positive so the statement above is

limited as clinical N.0 and M.0 may call for investigation. Lymphography can have false negatives

as can bone scans either by isotope or X-ray, hence the value, even if limited, of PAP testing.

A threshold of 1 cm in the short axis for the oval nodes, and 0.8 cm for the round nodes, has been

recommended as the criteria for the diagnosis of lymph node metastases  (47). Tiny foci of

metastatic cancer in lymph nodes will defy discovery, unless seen down the microscope.

High-resolution MRI with lymphotrophic ultra-small super-paramagnetic iron oxide particles ……

The presence of the nanoparticles causes normal nodal tissue to turn black, and because

malignant nodal tissue is unable to take up the agent, metastases will have a signal intensity

higher than normal nodes, even in those that do not meet the standard size criteria for metastasis,

again, if large enough.

Bone scintigraphy (Isotopic/nuclear med. scans) remains the most sensitive method of assessing

bone metastases, being superior to clinical evaluation, bone radiographs, serum alkaline

phosphatase measurement and prostatic acid phosphatase (PAP) determination. BK would like to

reread the references that suggest PAP has "prognostic significance")

The need for reliable serum markers to improve the pre-treatment staging of patients with PCa

has long been recognised.

using the more widely accepted Gleason score, and showed that the risk of PCa death was very

high in Gleason 7-10 tumours, intermediate in Gleason 6 tumours, but low in Gleason 2-5 cancers

(Table 9) (28, 29) (level of evidence: 3). This paper also showed that Gleason 6-10 tumours carry

a continuously increasing risk of ending the patientʼs life for up to 15 years of follow-up after

conservative management.

external irradiation offers the same long-term survival results as surgery; moreover, external

irradiation provides a quality of life at least as good as that provided by surgery

Radiotherapy affects erectile function to a lesser degree than surgery according to retrospective

surveys of patients (2). A recent meta-analysis has shown that the one-year rate of probability for

maintaining erectile function was 0.76 after brachytherapy, 0.60 after brachytherapy plus external

irradiation, 0.55 after external irradiation, 0.34 after nerve-sparing radical prostatectomy, and 0.25

after standard radical prostatectomy. When studies with more than two years of follow-up were

selected (i.e. excluding brachytherapy), the rates became 0.60, 0.52, 0.25, and 0.25, respectively,

with a greater spread between the radiation techniques and surgical approaches

Because of the hormonal dependence of prostate cancer (71), ADT has been combined with

external irradiation with the aim of:

• reducing the risk of distant metastases by potentially sterilising micrometastases already

present at the moment of diagnosis B.K. does not believe this.

 • decreasing the risk of non-sterilisation and/or local recurrence as a source of secondary

metastases (72) through the effect of radiation-induced apoptosis  (73, 74).

73. Zietman AL, Prince EA, Nakfoor BM, Park JJ. Androgen deprivation and radiation therapy:

sequencing studies using the Shionogi in vivo tumour system. Int J Radiat Oncol Biol Phys 1997;38

(5):1067-70. http://www.ncbi.nlm.nih.gov/pubmed/9276373

74. Joon DL, hasegawa M, Sikes C, Khoo VS, Terry NhA, Zagars GK, Meistrich M, Pollack A.

Supraadditive apoptotic response of R3327-G rat prostate tumours to androgen ablation and

radiation. Int J Radiat Oncol Biol Phys 1997;38(5):1071-7. http://www.ncbi.nlm.nih.gov/pubmed/

9276374 B.K. would like to see these two papers to see if there is avoidance that potentially

resting cancer cells suffer apotheosis, or just the dividing cells. If androgen deprivation slows/

stops cell division, dividing cells are at risk of ultimate death or by apotheosis, without affecting the

basic potential of cells to reenter dividing mode. Mind you, I was not much of a radiobiologist or

cell biologist either.

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