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Thread: Defining predictors of overall survival for high-risk men after RP

  1. #21
    Top User garyi's Avatar
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    Quote Originally Posted by DjinTonic View Post
    .......I'm afraid that for some this has become a game of Chicken.

    Djin
    Superb analogy!
    72...LUTS for the past 7 years
    TURP 2/16,
    G3+4 discovered
    3T MRI 5/16
    MRI fusion guided biopsy 6/16
    14 cores; four G 3+3, one G3+4,
    CIPRO antibiotic = C. Diff infection 7/16
    Cured with Vanco for 14 days
    Second 3T MRI 1/17
    Worsened bulging of posterior capsule
    Oncotype DX GPS 3/17, LFP risk 63%, Likelihood of Low
    Grade Disease 81%, Likelihood of Organ Confined 80%
    RALP 7/13/17 Dr. Gonzaglo @ Univ of Miami
    G3+4 Confirmed, Organ confined
    pT2 pNO pMn/a Grade Group 2
    PSA 0.32 to .54 over 3 months
    DCFPyl PET & ercMRI Scans - 11/17
    A one inch tumor still in prostate bed = failed surgery
    All met scans clear
    SRT, 2ADT, IMGT 70.2 Gys @1.8 per, completed 5/18
    Radiation Procitis, and Ulcerative Colitis flaired after 20 years
    PSA <.006 9/18, .054 11/18, .070 12/18, .067 2/19, .078 5/19, .074 7/19
    We'll see....what is not known dwarfs what is thought to be fact

  2. #22
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    Playing "chicken" isn't a very attractive option for people who have a low tolerance for risk! What I heard from my Doc today at Hopkins leads me to believe that he's not going to play that game. I successfully completed the 2 year clinical trial, but will remain on the "every 90 day PSA " schedule for two more years.
    2010-PSA 3.59; 2011-PSA 3.58; 2012-PSA 5.28, 4.26; 2013-PSA 5.98, 7.37; 2014-PSA 5.90, 4.70; 2015-PSA 5.18, 7.35
    RALP 16 March 17, Wesley Long, Greensboro, NC
    Pathology: pT3a, pN1 Gleason 4+5=9 adenocarcinoma with + surgical margin at bladder neck; 3 of 16 lymph nodes positive; neg seminal vesicles, vasa deferens
    Referral to Dr. Ken Pienta, Clinical Dir Research, Brady Center, Johns Hopkins
    Enrolled in Clinical Trial IRB002120414 “Phase II Study of definitive therapy for oligometastatic prostate cancer post surgery"
    Completed: Docetaxel 12 Jun 17, 3 Jul 17, 24 Jul 17, 14 Aug 17, 15 Sep 17
    Lupron every 90 days for two years. Completed March 2019
    Bone/Body Scans - 15 Sep 17 - neg; 15 Mar 18 - neg; 14 Sep 18 - neg; 17 Mar 19 - neg
    EBRT: 69 Gy total (46 to fossa, 23 boost to suspect areas) 1st treatment 28 Sep 17, last 22 Nov 17
    PSA: 25 May 17=0.2; 5 Sep 17=0.1; 18 Dec 17=0.1; 6 Mar 18=0.1; 29 May 18=0.1; 5 Sep 18=0.1; 17 Dec 18=0.1; 12 Mar 19=0.1; 15 Jul=0.1

  3. #23
    Quote Originally Posted by BAB View Post
    Playing "chicken" isn't a very attractive option for people who have a low tolerance for risk! What I heard from my Doc today at Hopkins leads me to believe that he's not going to play that game. I successfully completed the 2 year clinical trial, but will remain on the "every 90 day PSA " schedule for two more years.
    I wasn't referring to adjuvant treatment after RP. When that is deemed necessary it's done without regard to post-op PSA. I was referring to basically pT2 men like me with basically prostate-confined PCa, who don't have any more reason to believe the BCR source is in the prostate bed than in lymph nodes or other mets.

    Djin
    69 yr at Dx, BPH x 20 yr, 9 (!) neg. Bx, PCA3 -
    2013 TURP (90→30 g) path neg. then 6-mo. checks
    6-06-17 Nodule on R + PSA rise on finasteride: 3.6→4.3
    6-28-17 Bx #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 3% RLM
    Bone scan, CTs, X-rays: neg.
    8-7-17 Open RP, neg. frozen sections, Duke Regional
    SM EPE BNI LVI SVI LNI(16): negative, PNI+, nerves spared
    pT2c pN0 pMX acinar adenocarcinoma G9 (4+5) 5% of prostate (4.5x5x4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%, 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 wk) PSA <0.1
    LabCorp uPSA, Roche ECLIA:
    11-28-17 (3 m ) 0.010
    02-26-18 (6 m ) 0.009
    05-30-18 (9 m ) 0.007
    08-27-18 (1 yr.) 0.018 (?)
    09-26-18 (13 m) 0.013 (30-day check)
    11-26-18 (15 m) 0.012
    02-25-19 (18 m) 0.015
    05-22-19 (21 m) 0.015

  4. #24
    Senior User
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    Quote Originally Posted by DjinTonic View Post
    I also would be in the intermediate group. According to that study a G8 pT3b patient with a PSA <10 would be lower risk than a G7 pT2a with a PSA >10. Not likely.
    DOB 5/1957

    PSA - 11/2010=1.9, 6/12=2.3, 12/13=2.19, 12/14=2.64, 3/17=5.29, 3/17=3.91, 6/17=3.47, 12/17=4.50, 12/17=3.80, free PSA low risk (local (Uro, “My opinion you don’t have cancer), 8/18=5.13, 10/18=5.1, 10/19 ISO PSA 56% risk cancer. All DREs negative.

    DX 12/18, GS 8, 4+4 6/12 cores, LL Apex 100%, LM Apex 60%, LL Mid 50%, LMM 40%, LL Base 5%, LM <5%, Right side negative, (Uro opinion “This has been going on for a year”.... ah, more like 2 years ). Bone scan/CT negative

    2/25/19 R-LESS (Robotic Laparoendoscopic Single Site Surgery) outpatient Cleveland Clinic,

    3/6/19. Pathology - Grade Group 4 with Intraductal Carinoma
    T3aNO, GS8, 21 mm unifocal tumor 10%. -7 Nodes, - SV, - Margins, - PNI,
    - bladder neck neg., +LVI, + EPE non focal apex/mid lateral 1mm max extension, Cribriform pattern present. Decipher .86 High Risk.

    PSA 3/27/19 .03. (29 days)
    4/25/19 <.03. (58 days)
    5/25/19 <.02. (88 days)

    ADT - 6/3/19
    ART - 8/5/19

  5. #25
    Quote Originally Posted by Duck2 View Post
    I also would be in the intermediate group. According to that study a G8 pT3b patient with a PSA <10 would be lower risk than a G7 pT2a with a PSA >10. Not likely.
    We now know from genomics e.g., the Decipher test, that Low, Avg. And High metastatic risk cuts across all Gleason scores.

    A Low-Risk or Avg. G8 could be pT3 because it spread into (perhaps just a small portion of) a seminal vesicle. That makes it locally advanced, but in some cases cured with primary or primary+SRT. The lower PSA might be a marker it is still entirely local.

    An Avg. or High Risk G7 pT2 may have already have PCa cells with metastatic capability in the bloodstream or lymphatic system (or even established micromets) before primary treatment. The higher PSA could be evidence of this likelihood. We know that being pT2 is no guarantee that primary treatment will be a cure.

    Intuition is fine for formulating hypotheses, but we shouldn't dismiss results outright because they go against intuition. This was just one study (with about 1000 cases) that led to proposed risk groups based on statistics. This risk-group proposal may pan out after future studies or it may not.

    This study was done "way back" in 2015. Perhaps adding a genomic test to the criteria would make the risk groups even more accurate.

    If you ask me if I would trade my current status as a surgically treated PSA < 10, G9, pT2 with a very good path report and low met risk, for, say, a treated PSA > 10, G7, pT3b with a very poor path report and high met risk, how should I answer? There are so many factors and we don't really know which combinations count more than others. They study in question proposes we use stats to identify the significant combos.

    Djin
    Last edited by DjinTonic; 07-16-2019 at 11:14 AM.
    69 yr at Dx, BPH x 20 yr, 9 (!) neg. Bx, PCA3 -
    2013 TURP (90→30 g) path neg. then 6-mo. checks
    6-06-17 Nodule on R + PSA rise on finasteride: 3.6→4.3
    6-28-17 Bx #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 3% RLM
    Bone scan, CTs, X-rays: neg.
    8-7-17 Open RP, neg. frozen sections, Duke Regional
    SM EPE BNI LVI SVI LNI(16): negative, PNI+, nerves spared
    pT2c pN0 pMX acinar adenocarcinoma G9 (4+5) 5% of prostate (4.5x5x4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%, 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 wk) PSA <0.1
    LabCorp uPSA, Roche ECLIA:
    11-28-17 (3 m ) 0.010
    02-26-18 (6 m ) 0.009
    05-30-18 (9 m ) 0.007
    08-27-18 (1 yr.) 0.018 (?)
    09-26-18 (13 m) 0.013 (30-day check)
    11-26-18 (15 m) 0.012
    02-25-19 (18 m) 0.015
    05-22-19 (21 m) 0.015

  6. #26
    Senior User
    Join Date
    Jan 2019
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    479
    Quote Originally Posted by DjinTonic View Post
    We now know from genomics e.g., the Decipher test, that Low, Avg. And High metastatic risk cuts across all Gleason scores.

    A Low-Risk or Avg. G8 could be pT3 because it spread into (perhaps just a small portion of) a seminal vesicle. That makes it locally advanced, but in some cases cured with primary or primary+SRT. The lower PSA might be a marker it is still entirely local.

    An Avg. or High Risk G7 pT2 may have already have PCa cells with metastatic capability in the bloodstream or lymphatic system (or even established micromets) before primary treatment. The higher PSA could be evidence of this likelihood. We know that being pT2 is no guarantee that primary treatment will be a cure.

    Intuition is fine for formulating hypotheses, but we shouldn't dismiss results outright because they go against intuition. This was just one study (with about 1000 cases) that led to proposed risk groups based on statistics. This risk-group proposal may pan out after future studies or it may not.

    This study was done "way back" in 2015. Perhaps adding a genomic test to the criteria would make the risk groups even more accurate.

    If you ask me if I would trade my current status as a surgically treated PSA < 10, G9, pT2 with a very good path report and low met risk, for, say, a treated PSA > 10, G7, pT3b with a very poor path report and high met risk, how should I answer? There are so many factors and we don't really know which combinations count more than others. They study in question proposes we use stats to identify the significant combos.

    Djin
    I suppose it is my psychology, but I have yet to be convinced any T3 with >4+3 is curable.

    Sure, you may remain undetectable die of something else first, but if you were to live long enough the cancer will be detectable at some point.
    DOB 5/1957

    PSA - 11/2010=1.9, 6/12=2.3, 12/13=2.19, 12/14=2.64, 3/17=5.29, 3/17=3.91, 6/17=3.47, 12/17=4.50, 12/17=3.80, free PSA low risk (local (Uro, “My opinion you don’t have cancer), 8/18=5.13, 10/18=5.1, 10/19 ISO PSA 56% risk cancer. All DREs negative.

    DX 12/18, GS 8, 4+4 6/12 cores, LL Apex 100%, LM Apex 60%, LL Mid 50%, LMM 40%, LL Base 5%, LM <5%, Right side negative, (Uro opinion “This has been going on for a year”.... ah, more like 2 years ). Bone scan/CT negative

    2/25/19 R-LESS (Robotic Laparoendoscopic Single Site Surgery) outpatient Cleveland Clinic,

    3/6/19. Pathology - Grade Group 4 with Intraductal Carinoma
    T3aNO, GS8, 21 mm unifocal tumor 10%. -7 Nodes, - SV, - Margins, - PNI,
    - bladder neck neg., +LVI, + EPE non focal apex/mid lateral 1mm max extension, Cribriform pattern present. Decipher .86 High Risk.

    PSA 3/27/19 .03. (29 days)
    4/25/19 <.03. (58 days)
    5/25/19 <.02. (88 days)

    ADT - 6/3/19
    ART - 8/5/19

  7. #27
    Quote Originally Posted by Duck2 View Post
    I suppose it is my psychology, but I have yet to be convinced any T3 with >4+3 is curable.

    Sure, you may remain undetectable die of something else first, but if you were to live long enough the cancer will be detectable at some point.
    I suggest a revised philosophy or at least "working attitude" for life re PCa. Imagine (A ) reaching 96 and saying "Gee, I would have been so much happier not worrying about that all those years after all." Or, (B) at age whatever, PSA does rise, or the cancer does come back. You'll treat it. So it's not a total surprise; you were expecting it. Then how did worrying and casting a shadow on the time before that help you in any way at all--then or now?

    In other words, in one view, pessimism is nothing more than a choice with a downside only. Likewise optimism may be a self-fulfilling prophesy with an upside only. If it turns out not to get you to age 96, so be it--it served its purpose. I think it pays to try it out. You don't always know how much of your emotions and attitudes are under your control. Any PSA test could be the start of my BCR. I'll deal with it (I'll won't have much choice). But then, not now.

    I say this for anyone granted what may be a cure or just a reprieve.

    Djin

  8. #28
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    Quote Originally Posted by DjinTonic View Post
    As I have mentioned, Johns Hopkins proposed 0.4 for BCR; 0.2 was settled on in the main. One problem with very, or just early, treatment below 0.2 is that some men level off and won't reach 0.2 if left untreated (we don't know who, though). Compounding that issue is the one of benefit -- we are still awaiting the results of studies designed to answer the questions about adjuvant vs salvage RT; we don't really know which categories of men benefit from which timing. Thirdly, where do you treat? Why would I want my prostate fossa irradiated if the source of my new PSA rise is a met in my femur? Even the new, very sensitive PSMA-PET scans aren't good enough to detect lesions as such low PSA values.

    Let's assume my PSA starts to climb up from its current 0.015, for argument's sake, at a steady or even increasing pace. 0.03, 0.04, 0.06... Do I wait for a much higher PSA, even around 0.5 and get a newer scan? Do I irradiate the fossa sooner (at 0.1?) hoping the source is there? We in the Forum are used to see rising uPSA values that are quite small -- SRT at 0.5 or even higher is still considered "early" in many studies! We are in a transition period, I think, without good answers. I'm afraid that for some this has become a game of Chicken.

    Djin
    One consideration is the chance of your BCR being remote increases with the grade of your cancer i.e. 9 and 10, pretreatment PSA, genetic profile, and if treatment was early or late. Intermediate or low, not so much. And, if surgery was your primary treatment then the possibility it resides as well in the bed is a higher risk. Consider the entire profile.

    Then there is what is available to you to do? Radiaiting the bed is always a better safe than sorry even if distant mets live to fight another day. If you are a younger man you may want to consider a more aggressive approach.

    Another view is the data be used to support treatment, not to dismiss or avoid treatment. Everything appears different from the other side of the table. We see this often here where denial and delay are the real risks to interpretation and action.

    Less is more when it comes to sharpening the pencil. This is a fat pencil disease for the undisciplined mind, imo. I do think AI will be able to handle this if we can generate enough data.
    Last edited by Another; 07-16-2019 at 02:01 PM.
    Born 1953
    family w/PCa; grandfather, 3 brothers
    07-12-04 PSA 1.90
    07-10-06 PSA 2.02
    08-30-07 PSA 3.20
    12-01-11 PSA 5.69 Internist recommends urologist, I say no
    05-16-12 PSA 4.76 manipulate w/diet & supplements
    12-11-12 PSA 5.20, Health system changes to 3 years on testing
    03-07-16 PSA 7.20 Internist adamant on urologist
    DRE smooth, enlarged
    03-14-16 TRUS biopsy-prostatic adenocarcinoma 1%-60% across 8 of 12 samples, Gleason 3+3=6
    03-31-16 MRI pelvis w/o dye
    05-04-16 DaVinci prostatectomy, nerve sparing, Dr. Kent Adkins - recommend
    Final Path; weight 65g, lymph nodes, seminal vesicles, capsule, margin all negative, Gleason 3+4=7, Tumor volume 35%, +pT2c
    Catheter out - 16 days
    Incontinence at 6mos is minimal – no pad
    Cialis 3x/wk & Viagra on occasion
    Begin self-injection needle therapy for erections, stop after 6 due to onset of Peyronie’s
    Erections 100% - 14 months
    5-21-19 PSA <0.02, Zero Club 3.5 years

  9. #29
    Quote Originally Posted by Another View Post
    One consideration is the chance of your BCR being remote increases with the grade of your cancer i.e. 9 and 10, pretreatment PSA, and if treatment was early or late. Intermediate or low, not so much. And, if surgery was your primary treatment then the possibility it resides as well in the bed is a higher risk. Consider the entire profile.

    Then there is what is available to you to do? Radiaiting the bed is always a better safe than sorry even if distant mets live to fight another day. If you are a younger man you may want to consider a more aggressive approach.
    I think that until recently your argument had more merit. I'll reiterate two findings that now enter the picture, at least for my reasoning. (1) We used to think that metastatic potential was correlated only with G score. Now we have a good deal of data that shows exactly how low, avg. and high risk cut across G score (yes, the percentages for each of the 3 risk groups does vary with the G score). (2) The newer PSMA-PET scans are excellent at detecting PSA sources whether in the bed, regional lymph nodes, or distant nodes and mets. However they are at their sensitivity improves with increasing PSA, and they can still miss lesions as the very low uPSA values (below 0.2) that we are focusing on. This, too, should improve with time (they are still testing for the best isotope to use, currently Gallium and Flouride isotypes are duking it out, and I think in not too long, we'll have sensitivities that may redefine BCR entirely).

    Let's take my case. My uro/surgeon said after surgery that there were no problems removing my prostate ("It practically popped out" were his exact words). Since the operation was 4 hours (including wait time for frozen sections that came back negative), I'll take that non quite as a "pop", but rather relatively speaking: that he meant he encountered no "iffy" looking/feeling/perhaps-cancerous tissue and that the prostate wasn't particularly embeded in connective/fibrous tissue and whatever else makes removal harder. Bottom line points (hopefully) to a fairly good chance of no remaining prostate tissue. Decipher points to low risk of mets. So what's the likely source of the BCR that I might encounter?

    My decision may be not to jump at a very early PSA rise, but to wait for a reasonably diagnostic PSA level to do a scan, then decide if/where to irradiate. One Ga68-PSMA-PET study showed that in 25% of men with local, metastatic PCA after SRT the RT missed positive a pelvic node(s) because the field was too small. Knowing where the positive nodes are obviously helps. Of course when BCR happens is also a factor. If next year (age 72), then longer-term RT effects matter to me more than if I am, say, 85. I'm not saying no to RT of the bed, just that I want to be judicious in timing and testing to make the most of salvage treatment. Perhaps in the near future Circulating Tumor Cell measurements, improved imaging, and who knows what else will make a small delay smart. I would add that some (most?) centers of excellence for PCa still use a one-decimal PSA test, so jumping on SRT for changes in decimal places father out isn't even a choice. You can push the PSA trigger so small that you may as well just get adjuvant RT after your RP "just in case" in situations when that is not medically sound advice.

    We're discussing SRT simply because it's the most common treatment. Of course I'll be open to whatever treatments are proposed at the time. The reverse side of the coin holds true also: no reason for chemo if the recurrence is identified and is entirely in the prostate bed!
    Last edited by DjinTonic; 07-16-2019 at 02:42 PM.
    69 yr at Dx, BPH x 20 yr, 9 (!) neg. Bx, PCA3 -
    2013 TURP (90→30 g) path neg. then 6-mo. checks
    6-06-17 Nodule on R + PSA rise on finasteride: 3.6→4.3
    6-28-17 Bx #10: 2/14 cores: G10 (5+5) 50% RB, G9 (4+5) 3% RLM
    Bone scan, CTs, X-rays: neg.
    8-7-17 Open RP, neg. frozen sections, Duke Regional
    SM EPE BNI LVI SVI LNI(16): negative, PNI+, nerves spared
    pT2c pN0 pMX acinar adenocarcinoma G9 (4+5) 5% of prostate (4.5x5x4 cm, 64 g)
    11-10-17 Decipher 0.37 Low Risk: 5-yr met risk 2.4%, 10-yr PCa-specific mortality 3.3%
    Dry; ED OK with sildenafil
    9-16-17 (5 wk) PSA <0.1
    LabCorp uPSA, Roche ECLIA:
    11-28-17 (3 m ) 0.010
    02-26-18 (6 m ) 0.009
    05-30-18 (9 m ) 0.007
    08-27-18 (1 yr.) 0.018 (?)
    09-26-18 (13 m) 0.013 (30-day check)
    11-26-18 (15 m) 0.012
    02-25-19 (18 m) 0.015
    05-22-19 (21 m) 0.015

  10. #30
    Top User
    Join Date
    Aug 2016
    Posts
    1,653
    Quote Originally Posted by DjinTonic View Post
    I think that until recently your argument had more merit. I'll reiterate two findings that now enter the picture, at least for my reasoning. (1) We used to think that metastatic potential was correlated only with G score. Now we have a good deal of data that shows exactly how low, avg. and high risk cut across G score (yes, the percentages for each of the 3 risk groups does vary with the G score). (2) The newer PSMA-PET scans are excellent at detecting PSA sources whether in the bed, regional lymph nodes, or distant nodes and mets. However they are at their sensitivity improves with increasing PSA, and they can still miss lesions as the very low uPSA values (below 0.2) that we are focusing on. This, too, should improve with time (they are still testing for the best isotope to use, currently Gallium and Flouride isotypes are duking it out, and I think in not too long, we'll have sensitivities that may redefine BCR entirely).

    Let's take my case. My uro/surgeon said after surgery that there were no problems removing my prostate ("It practically popped out" were his exact words). Since the operation was 4 hours (including wait time for frozen sections that came back negative), I'll take that non quite as a "pop", but rather relatively speaking: that he meant he encountered no "iffy" looking/feeling/perhaps-cancerous tissue and that the prostate wasn't particularly embeded in connective/fibrous tissue and whatever else makes removal harder. Bottom line points (hopefully) to a fairly good chance of no remaining prostate tissue. Decipher points to low risk of mets. So what's the likely source of the BCR that I might encounter?

    My decision may be not to jump at a very early PSA rise, but to wait for a reasonably diagnostic PSA level to do a scan, then decide if/where to irradiate. One Ga68-PSMA-PET study showed that in 25% of men with local, metastatic PCA after SRT the RT missed positive a pelvic node(s) because the field was too small. Knowing where the positive nodes are obviously helps. Of course when BCR happens is also a factor. If next year (age 72), then longer-term RT effects matter to me more than if I am, say, 85. I'm not saying no to RT of the bed, just that I want to be judicious in timing and testing to make the most of salvage treatment. Perhaps in the near future Circulating Tumor Cell measurements, improved imaging, and who knows what else will make a small delay smart. I would add that some (most?) centers of excellence for PCa still use a one-decimal PSA test, so jumping on SRT for changes in decimal places father out isn't even a choice. You can push the PSA trigger so small that you may as well just get adjuvant RT after your RP "just in case" in situations when that is not medically sound advice.

    We're discussing SRT simply because it's the most common treatment. Of course I'll be open to whatever treatments are proposed at the time. The reverse side of the coin holds true also: no reason for chemo if the recurrence is identified and is entirely in the prostate bed!
    To state in a simpler way, you had no adverse conditions and will not benefit from early (0.03) salvage radiation treatment.

    To further my point of a simple consideration; while having a high G score; you had early detection (low volume and confined) and early treatment. And, your good fortune of location.

    The low risk may reside in free floating cells which seems to take time to establish and which was/is thwarted by your early detection and treatment.

    What surprises me is the Decipher score and before I relied on it to avoid treatment I'd want it to be based on more population data to establish more certainty. Does a decphher score within an individual's Gleason grade change with time? Another way, would your 4 and 5 graded cancer cells have developed the capacity to metatstisize with time and more generations/ Does an aggressive cell's ability to metastisize increase with it's newer generations? Then is there a mature limit to aggressiveness within a grade?

    The "popping out" you refer to is cancer cells are sticky and those breaching the tissue type they reside in make it difficult to detach from the healthy tissue. A surgeon's perspective on "confined." The hard boiled egg was easy to peel.
    Born 1953
    family w/PCa; grandfather, 3 brothers
    07-12-04 PSA 1.90
    07-10-06 PSA 2.02
    08-30-07 PSA 3.20
    12-01-11 PSA 5.69 Internist recommends urologist, I say no
    05-16-12 PSA 4.76 manipulate w/diet & supplements
    12-11-12 PSA 5.20, Health system changes to 3 years on testing
    03-07-16 PSA 7.20 Internist adamant on urologist
    DRE smooth, enlarged
    03-14-16 TRUS biopsy-prostatic adenocarcinoma 1%-60% across 8 of 12 samples, Gleason 3+3=6
    03-31-16 MRI pelvis w/o dye
    05-04-16 DaVinci prostatectomy, nerve sparing, Dr. Kent Adkins - recommend
    Final Path; weight 65g, lymph nodes, seminal vesicles, capsule, margin all negative, Gleason 3+4=7, Tumor volume 35%, +pT2c
    Catheter out - 16 days
    Incontinence at 6mos is minimal – no pad
    Cialis 3x/wk & Viagra on occasion
    Begin self-injection needle therapy for erections, stop after 6 due to onset of Peyronie’s
    Erections 100% - 14 months
    5-21-19 PSA <0.02, Zero Club 3.5 years

 

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