Prostate ...

Isaacs JT, D'Antonio JM, Chen S, et al. Adaptive auto-regulation of androgen receptor provides a paradigm shifting rationale for bipolar androgen therapy (BAT) for castrate resistant human prostate cancer. Prostate 2012;72(14):1491-505. http://onlinelibrary.wiley.com/doi/10.1002/pros.22504/abstract

Cell culture/xenograft and gene arrays of clinical material document that development of castration resistant prostate cancer (CRPC) cells involves acquisition of adaptive auto-regulation resulting in >25-fold increase in Androgen Receptor (AR) protein expression in a low androgen environment. Such adaptive AR increase paradoxically is a liability in castrated hosts, however, when supraphysiologic androgen is acutely replaced. Cell synchronization/anti-androgen response is due to AR binding to replication complexes (RC) at origin of replication sites (ORS) in early G1 associated with licensing/restricting DNA for single round of duplication during S-phase. When CRPC cells are acutely exposed to supraphysiologic androgen, adaptively increased nuclear AR is over-stabilized, preventing sufficient degradation in mitosis, inhibiting DNA re-licensing, and thus death in the subsequent cell cycle. These mechanistic results and the fact that AR/RC binding occurs in metastatic CRPCs directly from patients provides a paradigm shifting rationale for bipolar androgen therapy (BAT) in patient progressing on chronic androgen ablation. BAT involves giving sequential cycles alternating between periods of acute supraphysiologic androgen followed by acute ablation to take advantage of vulnerability produced by adaptive auto-regulation and binding of AR to RC in CRPC cells. BAT therapy is effective in xenografts and based upon positive results has entered clinical testing.


Denmeade SR, Isaacs JT. Bipolar androgen therapy: the rationale for rapid cycling of supraphysiologic androgen/ablation in men with castration resistant prostate cancer. Prostate 2010;70(14):1600-7. http://onlinelibrary.wiley.com/doi/10.1002/pros.21196/abstract

Androgen ablation is highly effective palliative therapy for metastatic prostate cancer but eventually all men relapse. New findings demonstrating that androgen receptor (AR) expression continues in androgen ablated patients has resulted in the classification "Castration Resistant Prostate Cancer" (CRPC) and has led to the development of new second-line "anti-ligand" hormonal agents. In this background is the paradoxical observation that the growth of some AR-expressing "androgen sensitive" human prostate cancer cells can be inhibited by supraphysiologic levels of androgens. This response may be due to effects of high-dose androgen on inhibiting re-licensing of DNA in cells expressing high levels of AR. It may also be due to recently described effects of androgen in inducing double strand DNA breaks. Based on available preclinical data described in this review demonstrating the effects of supraphysiologic levels of testosterone on inhibition of growth of CRPC xenografts, we initiated a clinical trial in men with CRPC testing the effect of monthly treatments with an intramuscular (IM) depot injection of testosterone. This IM formulation achieves supraphysiologic levels of testosterone that cannot be achieved with standard testosterone gel-based applications. The supraphysiologic testosterone level is followed by a rapid drop to castrate levels of testosterone with each cycle of therapy. This "bipolar androgen therapy" will not allow time for prostate cancer cells to adapt their AR expression in response to environmental conditions. The goal is to determine if a clinical response can be achieved through this non-adaptive rapid cycling approach in men with CRPC.
 
Re: Ultrasound to detect prostate cancer

Public release date: 8-Dec-2010
[ Print | E-mail | Share Share ] [ Close Window ]

Contact: Ivo Jongsma
i.l.a.jongsma@tue.nl
31-402-472-110
Eindhoven University of Technology
Accurate diagnosis of prostate cancer with ultrasound



IMAGE: Massimo Mischi, Ph.D., of Eindhoven University of Technology developed a new technology to accurately diagnose prostate cancer.
Click here for more information.




Prostate cancer is the most common type of cancer among men, but its diagnosis has up to now been inaccurate and unpleasant. Researchers at Eindhoven University of Technology (TU/e), in cooperation with AMC Amsterdam, have developed an imaging technology that can accurately identify tumors. The technology is based on ultrasound, and also has the potential to assess how aggressive tumors are. This can lead to better and more appropriate treatment, and to cost savings in health care.

About 11% of men who die of cancer in the western world do so as a result of prostate cancer. Each year 200,000 men are diagnosed with the disease in the US alone. But diagnosis is still rudimentary. After determining the PSA (prostate-specific antigen) level in the blood-, biopsies are performed to see if there are tumors in the prostate. However the PSA level is not a very good indicator: two-thirds of all biopsies turn out to afterwards to have been unnecessary.

The biopsies also have disadvantages; for example they are not targeted, but instead tissue is sampled randomly using 6 to 12 needles. The chance that the needles will miss a tumor is high, causing a false negative result. In around one-third of cases with negative biopsies, tumors are later found to be present. Furthermore doctors often operate after a positive biopsy, but find a tumor so small that it would have been better not to operate.

The new technology uses the injection of microbubbles of a contrast agent with no side-effects. The response of the tiny bubbles to ultrasound is different from that of human tissue or blood. This makes the bubbles traceable from the outside, right into the smallest blood vessels. The pattern of blood vessels in tumors is different from that in healthy tissue. The researchers can recognize this pattern from advanced analysis of the bubble concentrations. And because tumors need blood – and hence new blood vessels – to grow, the researchers expect to be able to see how aggressive the cancer is from the pattern of the blood vessels.

The technology has been tested on four patients from whom the affected prostate was removed, dr.ir. Massimo Mischi of the TU/e department of Electrical Engineering explains. The location and size of the tumors turned out to match accurately with the images produced using the new technology. Mischi presented these first, promising results at a recent conference in Chicago.

Next year the research team will carry out a pilot with biopsies guided by images made using the new technology. This allows the biopsies to be targeted, and therefore more effective. In a later phase the ultrasound technology will be used to decide whether biopsies are required, which will reduce the number of biopsies carried out. The researchers expect their technology to be available in hospitals within five years. The ultimate goal is for doctors to be able to determine if an operation is necessary, and if so what kind of operation, based on the images produced, without the need for biopsies.

All in all doctors will eventually be able to intervene much more accurately, expects prof.dr.ir. Hessel Wijkstra, head of urology research at AMC Amsterdam. Wijkstra was appointed part-time professor of Hemodynamic Contrast Sonography at TU/e last month. Furthermore he believes that there will be less unnecessary operations. In some cases doctors may decide to leave small, non-aggressive tumors untouched and monitor these tumors, in cases where a tumor is not causing any symptoms and is not impairing the health of the patient. In these cases the health effects of surgery are worse than those of the tumor itself. A further positive effect of this new approach is that the total costs will be reduced.

As well as TU/e and the AMC Amsterdam, the Catharina Hospital in Eindhoven and a number of ultrasound companies are also involved in the research. Dr.ir. Massimo Mischi received a Vidi grant worth eur 800,000 from the NWO (Netherlands Organisation for Scientific Research) last year for this research. The research also receives financial support from the Cure for Cancer Foundation.

###
This an old reply,but i had PSA score of 11.4 in june of 2012 which was an increase from 5.5 done in jan that same year.The doc did an ultra sound and took 12 samples by biopsy and it came back high grade cancer.I started ADT therapy the next month and continued with that untill Jan 2013. I was treated with radiation seed implant in november 2012, a total of 66 seeds were implanted. 2 months later i had 25 external radiation treatments done in Jan 2013. my PSA retest in May 2013 was 0.1. I still havnt recovered my testerone levels since discontiuation of the ADT thearapy in Jan 2013.
 
Re: Ultrasound to detect prostate cancer

This an old reply,but i had PSA score of 11.4 in june of 2012 which was an increase from 5.5 done in jan that same year.The doc did an ultra sound and took 12 samples by biopsy and it came back high grade cancer.I started ADT therapy the next month and continued with that untill Jan 2013. I was treated with radiation seed implant in november 2012, a total of 66 seeds were implanted. 2 months later i had 25 external radiation treatments done in Jan 2013. my PSA retest in May 2013 was 0.1. I still havnt recovered my testerone levels since discontiuation of the ADT thearapy in Jan 2013.


If you will, keep us updated. Thanks.
 
I am seeing an endo August 5th,i will post my results.I am sure he will do bloodwork and see where all my hormone levels are. My TSH was high and my primary doc said i was hypo thyroid, dont know if this is because of the treatments or not,i have alway had a very high metabolism. Here are some levels i had from my visit with my primary in MAY.
LH 2.0
TT 32
FT 0.2
TSH 11.4
RBC 3.80
everthing else was in the normal range.CBC,Lipid panel,comp. metabolic panel.
 
Re: Ultrasound to detect prostate cancer

Man, Thats some hard core Sheyite...! So coming from a family history of two fathers before me having PC - help me here...

- I am guessing by "seed implant" this means the docs essentially inserted a cascade of "micropellets" with radioactive quality to kinda "cook" the cancer dead?? Is this correct?
- Do you have a central or peripheral type? Is it front or rear if peripheral? Side?
- How did the biopsies affect sex life?
- How do the implants affect sex life?
- Are there concerns of how this radiation treatment may affect other areas of the body?
- If so (or not) I Wonder how ejaculation may affect the process? Could it help to keep radioactivity isolated by "excreting" what is going on with this treatment as immediate to the prostate?
- Moving on considering sex is not affected yet - did semen change visually?
- Are there concerns not to ejaculate in wife while treatment is "active"?
- what are your thoughts?

I AM IGNORANT ONLY ASKING. So no offense. I am ASSUMING the treatment is designed as an attempt to preserve the prostate so that you can go on to have function from it, as we all know the prostate is essentially the "motherboard" for the orgasm feeling. And while it has a lot to do with erections, I suspect things like Caverject are ways around that issue if full removal is required. Or is it really? Whatever you want to share is appreciated...:)

This an old reply,but i had PSA score of 11.4 in june of 2012 which was an increase from 5.5 done in jan that same year.The doc did an ultra sound and took 12 samples by biopsy and it came back high grade cancer.I started ADT therapy the next month and continued with that untill Jan 2013. I was treated with radiation seed implant in november 2012, a total of 66 seeds were implanted. 2 months later i had 25 external radiation treatments done in Jan 2013. my PSA retest in May 2013 was 0.1. I still havnt recovered my testerone levels since discontiuation of the ADT thearapy in Jan 2013.
 
Re: Ultrasound to detect prostate cancer

Man, Thats some hard core Sheyite...! So coming from a family history of two fathers before me having PC - help me here...

- I am guessing by "seed implant" this means the docs essentially inserted a cascade of "micropellets" with radioactive quality to kinda "cook" the cancer dead?? Is this correct?
- Do you have a central or peripheral type? Is it front or rear if peripheral? Side?
- How did the biopsies affect sex life?
- How do the implants affect sex life?
- Are there concerns of how this radiation treatment may affect other areas of the body?
- If so (or not) I Wonder how ejaculation may affect the process? Could it help to keep radioactivity isolated by "excreting" what is going on with this treatment as immediate to the prostate?
- Moving on considering sex is not affected yet - did semen change visually?
- Are there concerns not to ejaculate in wife while treatment is "active"?
- what are your thoughts?

I AM IGNORANT ONLY ASKING. So no offense. I am ASSUMING the treatment is designed as an attempt to preserve the prostate so that you can go on to have function from it, as we all know the prostate is essentially the "motherboard" for the orgasm feeling. And while it has a lot to do with erections, I suspect things like Caverject are ways around that issue if full removal is required. Or is it really? Whatever you want to share is appreciated...:)
The problem with removing the prostrate is there is the possibility of not getting all the cancer cells,some may be in the tissue surounding prostrate. The sucess rate of getting all the cancer is the greatest doing the seed implant and external radiation,its in the 90 to 95% range.Prostrate removal is in the 50% range and you have the risk of having to use a bag straped to your leg to pee in the rest of your life.plus the seed implant and external radiation leaves the good prostate cells intact.The cancer cells are more easily destroyed by the radiation because they grow faster than prostaret cells.My cancer was in 2 places on the sides of the prostate,the seeds are titanium capsules a little smaller tha a grain of rice,he showed me one that he had incapsulated in a plastic cube.
The biopsy has no big deal it was painless,at least for me and its the only way to know for sure if its cancerous or not. The big problems are caused by the ADT which kils your test level to all most 0.It is used to shrink the prostrate(the smaller the prostrate the better the treatment is.Mine was never enlarged even with the 11.4 PSA is was normal size,it was checked numerous times and just before seed implants.I never had a problem urinating even when i did cycles with high dose of AAS.I have ED but im sure that is because i have no test,Cialis helps a little,i can orgasam but nothing comes out,it feels the same but nothing comes out.The only restriction after the seed implants was to not let children sit in my lap for 2 months after the implants,after that time the radiation is no longer active. The treatment i had was the absolute best choice,with the best sucess rate,with cancer still confined to the prostrate.I had CT scans to see if it had spread to other organs and a full body bone scan which came up negative.The most important thing is to catch it early while it is still confined to the prostrate.
Heres a link to the cancer center i went to,it is suppose to be the best in the country at treating prostrate cancer.My doctor was Dr Terk.
Florida Center For Prostate Care - Jacksonville, Florida
 
Garcia-Fontana B, Morales-Santana S, Varsavsky M, et al. Sclerostin serum levels in prostate cancer patients and their relationship with sex steroids. Osteoporos Int. Sclerostin serum levels in prostate cancer patients and their relationship with sex steroids - Online First - Springer

The role of sclerostin on bone metabolism and its relation to sex steroids in patients with prostate cancer (PC) is not well known. We found that sclerostin levels are significantly increased in PC patients, particularly in those with androgen deprivation therapy (ADT), and there is an inverse relationship between sclerostin levels and testosterone.

INTRODUCTION: Recent studies have evaluated sclerostin levels in bone diseases as osteoporosis. However, there are few data in PC patients, particularly in patients with hypogonadism related to ADT. The aim of the present study was to compare serum sclerostin levels in ADT/non-ADT-treated PC patients and healthy controls and to evaluate their relationship with sex steroids and bone metabolism.

METHODS: We performed a cross-sectional study involving 81 subjects: 25 ADT-treated PC patients, 34 PC patients without ADT treatment, and 22 healthy controls. We measured serum sclerostin levels, bone turnover markers, bone mineral density (BMD) in all individuals, and sex steroids levels in PC patients.

RESULTS: Serum sclerostin levels were significantly higher in PC patients compared to those in control subjects. ADT-treated patients had significantly higher sclerostin levels than PC patients without ADT treatment: ADT 64.52 +/- 27.21 pmol/L, non-ADT 48.24 +/- 15.93 pmol/L, healthy controls 38.48 +/- 9.19 pmol/L, p < 0.05. In PC patients, we found a negative relationship between serum sclerostin levels and androgens after age adjustment (total testosterone: r = -0.309, p = 0.029; bioavailable testosterone: r = -0.280, p = 0.049; free testosterone: r = -0.299, p = 0.035). We did not observe any relationship between sclerostin levels and bone turnover markers or BMD in any group.

CONCLUSIONS: Circulating sclerostin levels are significantly increased in patients with PC and particularly in those receiving ADT. The inverse relationship between serum sclerostin and testosterone in these patients suggests that androgens are key regulators of bone metabolism in this population.
 
Ryan CJ, Molina A, Li J, et al. Serum Androgens As Prognostic Biomarkers in Castration-Resistant Prostate Cancer: Results From an Analysis of a Randomized Phase III Trial. Journal of Clinical Oncology 2013;31(22):2791-8. Serum Androgens As Prognostic Biomarkers in Castration-Resistant Prostate Cancer: Results From an Analysis of a Randomized Phase III Trial

Purpose In the phase III study COU-AA-301, abiraterone acetate (AA) plus prednisone (P) prolonged overall survival (OS) in patients with metastatic castration-resistant prostate cancer (mCRPC) after docetaxel administration. In this article, we investigate the relationship between baseline serum androgen (SA) levels and OS.

Patients and Methods COU-AA-301 is a randomized, double-blind study of AA (1,000 mg every day) plus P (5 mg by mouth twice daily; n = 797) versus P alone (n = 398). Randomization was stratified by Eastern Cooperative Oncology Group performance status (0 to 1 v 2), pain (Brief Pain Inventory-Short Form over past 24 hours: 4 to 10, present; v 0 to 3, absent), prior chemotherapy (1 v 2), and progression (prostate-specific antigen v radiographic). Association of baseline SA (testosterone, androstenedione, dehydroepiandrosterone sulfate), was measured by ultrasensitive liquid-liquid extraction or protein precipitation and two-dimensional liquid chromatography coupled to mass spectrometry, with OS determined by bivariate and multivariable Cox models. OS was examined with SA as greater than median and less than or equal to the median.

Results Median survival increased with each quartile increase in testosterone level regardless of treatment arm. SA levels at baseline strongly associated with survival (P < .0001) in bivariate and multivariable analyses. Longer survival was observed for patients with SA above median compared with below median in both the AA and P arms (eg, testosterone, AA; hazard ratio, 0.64; 95% CI, 0.53 to 0.77; P < .0001). Treatment with AA led to longer survival versus P alone in the above- or below-median group for all androgens.

Conclusion SA, measured with a novel ultrasensitive assay in COU-AA-301, is prognostic for OS and may be useful for risk stratification in mCRPC clinical trials.
 
Few would disagree with the mission of providing the highest-value health care possible. Unfortunately, the consensus dissipates when a particular practice is targeted for elimination because it provides little or no value. Such is the state of the prostate-specific antigen (PSA) test for prostate cancer screening.

Although the US Preventive Services Task Force (USPSTF) recommended against its use for men 75 years or older in 20081 and in 2012 concluded that there is insufficient evidence to recommend routine screening for anyone, the test is still being ordered every day in every health care system including mine, reimbursed not only by private insurance but by public insurance (Medicare and Medicaid) and scarce county health dollars for the uninsured.

Why is this? If the test is so unhelpful, why are we not able to devote the money to higher-value care?

Katz MH. Can We Stop Ordering Prostate-Specific Antigen Screening Tests?. JAMA Intern Med. 2013;173(10):847-848. JAMA Network | JAMA Internal Medicine | Can We Stop Ordering Prostate-Specific Antigen Screening Tests?
 
Re: Ultrasound to detect prostate cancer

Thanks for the reply. I recall Dad had a catheter for about 6 months or so after surgery for complete removal. Maybe even a year. I am guessing the reason for the risk of permanent use of catheter is if the cancer is close to the bladder valve, or they damage nerves leading to/involved?? Cause they should be separate. He had his taken out at about 50 years old and still kicking today over 70. The ODD THING is that his uro states PSA is rising (slowly) over years and really does not know why. Its like, how can you have a PSA if you have no prostate to generate PSA!??!?? But still I don't think it over 0.2 at any time and no issues or indications of recurrence. So who knows. He got on a blueberry kick for a while that he claimed Zero'd it back out, but for some reason he gave that up- who knows why..

But sounds like you had a tough one to diagnose with no inflammation associated and that only an experienced touch could find. Fortunately it was in an area they could feel it to find it... So you are a case where PSA had some good diagnostic value.

Thoughts for me please...:
1. Did you suspect erections or ejaculation was suffering prior to diagnosis?
2. Did you have vasectomy younger and years prior?
3. What is your interpretation of the androgen blockage treatment (or whatever they formally call it). Is this a drug you take/took - and what?
4. Have they involved the seminal vessel (which I believe is above and away from the prostate) at this time. Which seeds or anything? Do you think you are even emitting seminal fluid at any time, or do you think production of that has shut down due to treatment?
5. I am assuming the removal of seminal vessel is part of full prostate removal of course. So it makes me wonder how/why this is effecting ejaculation volume if orgasming?

** I only ask about the seminal fluid deal as I am so used to seeing it run down my leg after about 3 hours post Adderall usage - LOL. I am really wondering how DOP/NE action on MY prostate is going to affect it long term..!??!??

On the flipside GRANDAD did not have his diagnosed till 75 and they pretty much tried to non-invasively treat his with blockage therapy at best I think. He lasted about 5 years and I recall seeing bone scans just black everywhere. Not pretty. This was back in 80's before men really gave shit about seeing uro's for checks. But the reality is I suspect he had same one my dad had and just lasted 25 years before it was an issue. Which is why I cant help but think I will be on the table at 50. Still dad smoked and was obese his whole life. So maybe he would not have got till 60-65 who knows... I need to go back now as early 40's and the thought just creeps me out just waiting for the day he starts digging around extended and I know what he is gonna come up saying (other than "boy you got a fat ass" - LOL[:o)])

Really, i just don't know what I will do if I loose my "orgasm sensation generator". That would be kinda like telling Richard Simmons that there is no more cake to eat:(:D. Personally, the simple pleasures are my bread&butter.. Yes - getting old SUCKS...

Best wishes again my thoughts are with you...!
:)


The problem with removing the prostrate is there is the possibility of not getting all the cancer cells,some may be in the tissue surounding prostrate. The sucess rate of getting all the cancer is the greatest doing the seed implant and external radiation,its in the 90 to 95% range.Prostrate removal is in the 50% range and you have the risk of having to use a bag straped to your leg to pee in the rest of your life.plus the seed implant and external radiation leaves the good prostate cells intact.The cancer cells are more easily destroyed by the radiation because they grow faster than prostaret cells.My cancer was in 2 places on the sides of the prostate,the seeds are titanium capsules a little smaller tha a grain of rice,he showed me one that he had incapsulated in a plastic cube.
The biopsy has no big deal it was painless,at least for me and its the only way to know for sure if its cancerous or not. The big problems are caused by the ADT which kils your test level to all most 0.It is used to shrink the prostrate(the smaller the prostrate the better the treatment is.Mine was never enlarged even with the 11.4 PSA is was normal size,it was checked numerous times and just before seed implants.I never had a problem urinating even when i did cycles with high dose of AAS.I have ED but im sure that is because i have no test,Cialis helps a little,i can orgasam but nothing comes out,it feels the same but nothing comes out.The only restriction after the seed implants was to not let children sit in my lap for 2 months after the implants,after that time the radiation is no longer active. The treatment i had was the absolute best choice,with the best sucess rate,with cancer still confined to the prostrate.I had CT scans to see if it had spread to other organs and a full body bone scan which came up negative.The most important thing is to catch it early while it is still confined to the prostrate.
Heres a link to the cancer center i went to,it is suppose to be the best in the country at treating prostrate cancer.My doctor was Dr Terk.
Florida Center For Prostate Care - Jacksonville, Florida
 
"But sounds like you had a tough one to diagnose with no inflammation associated and that only an experienced touch could find. Fortunately it was in an area they could feel it to find it... So you are a case where PSA had some good diagnostic value."
Actually the PSA score of 5.5 was the reason my primary doc sent me to a urologist.By the time i saw the urologist 4 months later it had risen to 11.4.The urologist did the ultra sound and biopsy the next month. The ultra sound lets the doc see the prostrate and see if there is any suspicious areas and then take samples from those areas.he wasnt just doing random samples of which he did 12 samples. The samples came back high grade cancer 7 on the scale.The biopsy was painless,they numbed the prostrate before they took any samples.Hardly any soreness the next day.
 
Last edited:
The problem with removing the prostrate is i believe they also remove the tube that comes from your bladder that goes through the middle of the prostrate.
The ADT therapy is called androgen depravation therapy.I went to the doc once a month for the shot that was given in the abdomen,it was a 30 day release version,i think he used the 30 release version instead of a 3 month or 6 month release version was because there are less side effects with the 30 day release version.IF i had to do it again i probably wouldnt do the ADT,there was also some pills you can take also with the shot to make it more effective but i decided not to use those It was optional..Th e purpose of ADT is to shrink the prostate and mine wasnt enlarged.I the seeds were implanted using ultra sound and a mapping of my prostrate to put them in the areas that need them.The external radiation treatment is very precise and targets only the prostrate,i had no side effects at all from the radiation treatments. Overall the experience was not bad and i didnt experience any pain except for the catheter for one day after the seed implants.
 
"On the flipside GRANDAD did not have his diagnosed till 75 and they pretty much tried to non-invasively treat his with blockage therapy at best I think. He lasted about 5 years and I recall seeing bone scans just black everywhere. Not pretty. This was back in 80's before men really gave shit about seeing uro's for checks. But the reality is I suspect he had same one my dad had and just lasted 25 years before it was an issue. Which is why I cant help but think I will be on the table at 50. Still dad smoked and was obese his whole life. So maybe he would not have got till 60-65 who knows... I need to go back now as early 40's and the thought just creeps me out just waiting for the day he starts digging around extended and I know what he is gonna come up saying (other than "boy you got a fat ass" - LOL)"
I was 66 when i had all this done,i was healthy and no medical issues so i didnt have a hard time with it.There were guys there getting the radiation treatments and also had other issues and were having a hard time. The nurse that talked to me said i was really doin very well to be 66 and not being on any kind of medication. I have no phisycal problems and not taking any kind of medication.I have also been doing steroids off and on for over 30 years.If you have low grade cancer you can do ADT and it will stop the cancer from growing,but for obvious reasons thats not prefered for someone like me and you,having no test is not something you would want.Im going to a endo monday and going to see what he will do about my low test situation, i may go TRT if he thinks it ok.
 
You ain't gonna find a Urologist on the planet (at least in these days) who's math is going to equate to PC +SYN-T ='s OK......

Really, one of my notions is that hormones are great until a cancer is in place, THEN THEY ARE JUST PART OF THE FUNDAMENTAL FEEDING AND GROWTH SYSTEM WHICH IS NOT GOOD IN CANCER CONDITIONS.

HOWEVER, if there are guys out there that can do TRT after complete and successful PC removal and not have issues - THEN THIS COULD BE THE PROOF THE TRT is indeed the fountain of youth and therefore PROTECTIVE...:)

"On the flipside GRANDAD did not have his diagnosed till 75 and they pretty much tried to non-invasively treat his with blockage therapy at best I think. He lasted about 5 years and I recall seeing bone scans just black everywhere. Not pretty. This was back in 80's before men really gave shit about seeing uro's for checks. But the reality is I suspect he had same one my dad had and just lasted 25 years before it was an issue. Which is why I cant help but think I will be on the table at 50. Still dad smoked and was obese his whole life. So maybe he would not have got till 60-65 who knows... I need to go back now as early 40's and the thought just creeps me out just waiting for the day he starts digging around extended and I know what he is gonna come up saying (other than "boy you got a fat ass" - LOL)"
I was 66 when i had all this done,i was healthy and no medical issues so i didnt have a hard time with it.There were guys there getting the radiation treatments and also had other issues and were having a hard time. The nurse that talked to me said i was really doin very well to be 66 and not being on any kind of medication. I have no phisycal problems and not taking any kind of medication.I have also been doing steroids off and on for over 30 years.If you have low grade cancer you can do ADT and it will stop the cancer from growing,but for obvious reasons thats not prefered for someone like me and you,having no test is not something you would want.Im going to a endo monday and going to see what he will do about my low test situation, i may go TRT if he thinks it ok.
 
Margel D, Urbach DR, Lipscombe LL, et al. Metformin Use and All-Cause and Prostate Cancer-Specific Mortality Among Men With Diabetes. Journal of Clinical Oncology. Metformin Use and All-Cause and Prostate Cancer–Specific Mortality Among Men With Diabetes

Purpose To evaluate the association between cumulative duration of metformin use after prostate cancer (PC) diagnosis and all-cause and PC-specific mortality among patients with diabetes.

Patients and Methods We used a population-based retrospective cohort design. Data were obtained from several Ontario health care administrative databases. Within a cohort of men older than age 66 years with incident diabetes who subsequently developed PC, we examined the effect of duration of antidiabetic medication exposure after PC diagnosis on all-cause and PC-specific mortality. Crude and adjusted hazard ratios (HRs) were calculated by using a time-varying Cox proportional hazard model to estimate effects.

Results The cohort consisted of 3,837 patients. Median age at diagnosis of PC was 75 years (interquartile range [IQR], 72 to 79 years). During a median follow-up of 4.64 years (IQR, 2.7 to 7.1 years), 1,343 (35%) died, and 291 patients (7.6%) died as a result of PC. Cumulative duration of metformin treatment after PC diagnosis was associated with a significant decreased risk of PC-specific and all-cause mortality in a dose-dependent fashion. Adjusted HR for PC-specific mortality was 0.76 (95% CI, 0.64 to 0.89) for each additional 6 months of metformin use. The association with all-cause mortality was also significant but declined over time from an HR of 0.76 in the first 6 months to 0.93 between 24 and 30 months. There was no relationship between cumulative use of other antidiabetic drugs and either outcome.

Conclusion Increased cumulative duration of metformin exposure after PC diagnosis was associated with decreases in both all-cause and PC-specific mortality among diabetic men.


Penney KL, Stampfer MJ. The Time Is Ripe for a Randomized Trial of Metformin in Clinically Localized Prostate Cancer. Journal of Clinical Oncology. The Time Is Ripe for a Randomized Trial of Metformin in Clinically Localized Prostate Cancer
 
First decent generic write-up I have seen to date...

That is pretty much how it was for me.the ultra sound and biopsy was painless and is pretty much the most reliable way to tell if its cancer or not.The only thing i would avoid if i had to do it again is the ADT shots,its not totally necessary and in some men it cant be used..........
 
That is pretty much how it was for me.the ultra sound and biopsy was painless and is pretty much the most reliable way to tell if its cancer or not.The only thing i would avoid if i had to do it again is the ADT shots,its not totally necessary and in some men it cant be used..........

That is interesting. IIRC, we had this discussion. How are you doing for T?
 
That is interesting. IIRC, we had this discussion. How are you doing for T?

I went to an endo monday with my labs from my primary doc which showed high TSH 11.4 and low TT-32 and low LH 2.0 and FT 0.2.He gave me some T4 88mcg to see what dose i will need,he said it is very common for men my age to have low thyroid.As for the test levels he told me " theres not an endo in town that will touch my testerone since i had Pca".......I have to get labs in 4 weeks to adjust my T4 level and he will check my TT also but i doubt he will do anything about my low test.I started 25mg Clomid and 20mg Nolvadex to see if i can get my test up for my labs to be done in 4 weeks.If he doesnt do anything for my test i will try to find someone who will.....As for ADT i never had a problem recovering my test after a cycle even a year or 2 ago after cycles when i was 64 and 65 years old. Its been 6 months since i stopped the ADT shots and i still havnt recovered despite HCG for a couple of weeks then a month of Clomid and Nolvadex.
 
Last edited:
Back
Top