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Guihan

Gleason 6 Treatment Options

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Guihan

When I was diagnosed with Gleason 6 PCa in 2003, I was advised by my urologist that this was a 'moderately aggressive cancer', and that radical prostatectomy was the best solution.

 

It seems that, in America at least, Gleason 6 is not now considered to be the beast it was once made out to be:

www.ascopost.com/issues/july-25-2018/when-can-patients-with-gleason-6-prostate-cancer-safely-undergo-active-surveillance/

 

I confess that I do not really understand this article. I suffered severe urinary incontinence at the time of my diagnosis, and my PSA was rising sharply. Three years after my RP, my PSA started rising again, and I calculated the doubling time at 67 days. I have been controlling it with ADT since that time.  Surely, the only practical options I had were RP or just ADT. I guess I will never know if ADT alone would have been sufficient, but how on earth would 'Active Surveillance' have been of any value in cases like mine?

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alanbarlee

  I agree with you that you took the right course of action back then. The very short PSADT of 2 months would make me doubt the reliability of the biopsy that came back with a GS 6 (which then was possibly only a 6-core sampling). I would also query your oncologist's description that GS 6 is 'moderately aggressive', unless that was after a higher post-RP GS result, but in the end your decision was good - I wouldn't have stood by and waited either.  

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Patrick Turner

Hi Guihan,

Having Psa doubling in 67 days or just over 2 months means that from little things, big things will grow, and grow very fast and become dangerous.

You have not said what your Psa is but watchful waiting or active surveillance might only be OK if Psa is below  the normal low range figure of 0.5 and it took 2 years to double. But if I had Psa at say 1.0, and it doubled in a year to 2.0, then to 3.0 in another 3 months, then knowing what I know now I would have had RP and PsMa scans and be ready to throw all I could at it.

But docs thought I was fine with Psa at 5.5, then biopsy at 6 a couple of months later gave Gleason 9, plus 9/9 positive biopsy samples. 4 months later the attempt at open RP was abandoned because of too much Pca outside PG so docs could not see what they were cutting, and might have spread my Pca more than it already had spread. If I had the biopsy 4 years before when Psa was 3, I might have been a lot better off than now. So the active surveillance practised on me by docs by simply saying I was OK because Psa > 5.5 was sheer bullshit. I was 62 at Dx, and for men who never will get Pca their Psa is about 1.0. Well how come no action is taken until Psa goes over 5 times the 1.0 figure ? It seems ridiculous to me, and possibly inspired by doctors preferring to avoid cheap early detection and prevention to make work for themselves in endless expensive Pca treatments and not curing anyone.

Numbers matter. 

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Guihan

Sorry - my old brain forgot to include my very first (pre-ADT) PCa doubling time calculation. I recorded nine increments in PSA before I did my first calculation in Sept 2007, so I was able to plot it very accurately. That gave me an initial doubling time of 187 days. Two tandem Zoladex implants then drove the PSA down to a sub-recordable value. My PSA subsequently broke out (became readable) again on four occasions, before being beaten down again each time by Zoladex. Sadly, it came back as a much more savage beast. On each of those post-ADT breakouts, I calculated the doubling time as a strangely consistent 66 or 67 days. I had not been warned that ADT could have that effect on my cancer doubling time.

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Guihan

Patrick, as far as I can remember, my pre-op. PSA level was about 9. Post-op., I got various (not very accurate) readings of 0.1 or 0.2 before the PSA took off in 2007, 3 years after my RP.

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alanbarlee

So - your initial PSDT was around 6 months, (with PSA getting up to 9 - a good time for starting the ADT). Even with a low risk biopsy GS of 3+3  (no RP Gleason mentioned), that growth rate would definitely have got my attention. A PSADT of 10 months or less is one rule of thumb for increasing risk, and is more often associated with at least some GS grade 4 - but not in your case, it seems, even after extended ADT reduced the doubling time to only 2 months. You appear to have been blessed with a single phenotype that may not have mutated and metastasised under the long-term selection pressure of the ADT.

 

Best wishes with the oral T - may you gain some improved muscle and bone, and be able to find your car keys again!

 

Alan   

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