Question about biopsy results

daveirving
daveirving Member Posts: 14
My last biopsy found one positive in 31 samples <5% G3+3=6. Am I right to assume that I could have a greater % of cancer and higher G in other areas of my prostate that the needles missed?
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Comments

  • Kongo
    Kongo Member Posts: 1,166 Member
    Certainly that is a possibility but very unlikely. As I recall you had two or three other biopsies with negative results. Given the size of your prostate the 31 cores is pretty much saturation. Most men (60% of men in their sixties) have some small amounts of prostate cancer cells in their prostate.

    Fortunately in your case all the indications you have mentioned point toward a very early or insolent form of prostate cancer.

    I would encourage you to read many of the excellent threads in this forum about diet, particularly dairy and red meat, and the relationship these foods have tp prostate cancer.
  • tarhoosier
    tarhoosier Member Posts: 195 Member
    Indolent
    Dave there is no reason, none, for you to go to primary treatment with the finding(s) that you present here. Based on the most thorough biopsy available you have nearly zero chance of a lethal type of prostate cancer. Watch, monitor, and save your body for other issues, is my advice.
  • hopeful and optimistic
    hopeful and optimistic Member Posts: 2,339 Member

    Indolent
    Dave there is no reason, none, for you to go to primary treatment with the finding(s) that you present here. Based on the most thorough biopsy available you have nearly zero chance of a lethal type of prostate cancer. Watch, monitor, and save your body for other issues, is my advice.

    agree
    when I was diagnosed with numbers slightly worse than you, I saw a world class robotic surgeon and the number one guy at UCLA. I had lots of questions to ask him about surgery, including the number of surgeries that he had done (a robotic surgeon needs to do a lot of them to becoming competent, otherwise the surgeon is learning on you).

    He looked at my numbers, told me that my cancer is indolent, not likely to spread and I am an excellent candidate for Active Surveillance, he mentioned a study or two to support this, then got up to leave. He only spoke for a very short time, maybe 5 minutes at most, and I had all these questions about surgery. On his way out, I asked him how many surgeries he had done. He stopped walking out, thought a moment, answered my question, and said, "I'm a world class surgeon, but you don't need surgery" and kept on walking.

    Now Dave.....that's the kind of surgeon that you need see....world class, and not self serving.
  • daveirving
    daveirving Member Posts: 14

    agree
    when I was diagnosed with numbers slightly worse than you, I saw a world class robotic surgeon and the number one guy at UCLA. I had lots of questions to ask him about surgery, including the number of surgeries that he had done (a robotic surgeon needs to do a lot of them to becoming competent, otherwise the surgeon is learning on you).

    He looked at my numbers, told me that my cancer is indolent, not likely to spread and I am an excellent candidate for Active Surveillance, he mentioned a study or two to support this, then got up to leave. He only spoke for a very short time, maybe 5 minutes at most, and I had all these questions about surgery. On his way out, I asked him how many surgeries he had done. He stopped walking out, thought a moment, answered my question, and said, "I'm a world class surgeon, but you don't need surgery" and kept on walking.

    Now Dave.....that's the kind of surgeon that you need see....world class, and not self serving.

    Thankyou for the info.
    I am going to call my Doctor at the Mayo and see if I he would recomend a AS specialist. When I first talked to My surgeon he was talkes about AS but I was not interested.
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member

    Thankyou for the info.
    I am going to call my Doctor at the Mayo and see if I he would recomend a AS specialist. When I first talked to My surgeon he was talkes about AS but I was not interested.

    Get second opinions from diferent specialists
    Dave

    My opinion as a layman on the info you have shared with us, is that AS may be proper to you if the PSA spike can be justified by other causes than PCa.
    The biopsy refers to a contained cancer (no other detaild regarding PIN or eExtension), small in volume and low grade in agressivity, but the PSA is high (7.8) for an indolent type of cancer. The PSADT is also too short and it should be considered in your diagnosis.
    Try to get second opinions from diferent specialists.

    Wishing you the best.

    VGama
  • wagz64
    wagz64 Member Posts: 1
    biopsy
    i had 16 samples taken and 7 positive ones
    were detected but when they went in it was a lot worst
  • hopeful and optimistic
    hopeful and optimistic Member Posts: 2,339 Member
    came across this study



    Role of prostate specific antigen and immediate confirmatory biopsy in predicting progression during active surveillance for low risk prostate cancer.

    Adamy A, Yee DS, Matsushita K, Maschino A, Cronin A, Vickers A, Guillonneau B, Scardino PT, Eastham JA.


    Source

    Urology Service, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. ariadamy@gmail.com


    Abstract

    PURPOSE:

    We evaluated predictors of progression after starting active surveillance, especially the role of prostate specific antigen and immediate confirmatory prostate biopsy.

    MATERIALS AND METHODS:

    A total of 238 men with prostate cancer met active surveillance eligibility criteria and were analyzed for progression with time. Cox proportional hazards regression was used to evaluate predictors of progression. Progression was evaluated using 2 definitions, including no longer meeting 1) full and 2) modified criteria, excluding prostate specific antigen greater than 10 ng/ml as a criterion.

    RESULTS:

    Using full criteria 61 patients progressed during followup. The 2 and 5-year progression-free probability was 80% and 60%, respectively. With prostate specific antigen included in progression criteria prostate specific antigen at confirmatory biopsy (HR 1.29, 95% CI 1.14-1.46, p <0.0005) and positive confirmatory biopsy (HR 1.75, 95% CI 1.01-3.04, p = 0.047) were independent predictors of progression. Of the 61 cases 34 failed due to increased prostate specific antigen, including only 5 with subsequent progression by biopsy criteria. When prostate specific antigen was excluded from progression criteria, only 32 cases progressed, and 2 and 5-year progression-free probability was 91% and 76%, respectively. Using modified criteria as an end point positive confirmatory biopsy was the only independent predictor of progression (HR 3.16, 95% CI 1.41-7.09, p = 0.005).

    CONCLUSIONS:

    Active surveillance is feasible in patients with low risk prostate cancer and most patients show little evidence of progression within 5 years. There is no clear justification for treating patients in whom prostate specific antigen increases above 10 ng/ml in the absence of other indications of tumor progression. Patients considering active surveillance should undergo confirmatory biopsy to better assess the risk of progression.

    Copyright © 2011 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.


    Comment in
    Nat Rev Urol. 2011 Feb;8(2):60.


    PMID: 21167529 [PubMed - indexed for MEDLINE]
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member

    came across this study



    Role of prostate specific antigen and immediate confirmatory biopsy in predicting progression during active surveillance for low risk prostate cancer.

    Adamy A, Yee DS, Matsushita K, Maschino A, Cronin A, Vickers A, Guillonneau B, Scardino PT, Eastham JA.


    Source

    Urology Service, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. ariadamy@gmail.com


    Abstract

    PURPOSE:

    We evaluated predictors of progression after starting active surveillance, especially the role of prostate specific antigen and immediate confirmatory prostate biopsy.

    MATERIALS AND METHODS:

    A total of 238 men with prostate cancer met active surveillance eligibility criteria and were analyzed for progression with time. Cox proportional hazards regression was used to evaluate predictors of progression. Progression was evaluated using 2 definitions, including no longer meeting 1) full and 2) modified criteria, excluding prostate specific antigen greater than 10 ng/ml as a criterion.

    RESULTS:

    Using full criteria 61 patients progressed during followup. The 2 and 5-year progression-free probability was 80% and 60%, respectively. With prostate specific antigen included in progression criteria prostate specific antigen at confirmatory biopsy (HR 1.29, 95% CI 1.14-1.46, p <0.0005) and positive confirmatory biopsy (HR 1.75, 95% CI 1.01-3.04, p = 0.047) were independent predictors of progression. Of the 61 cases 34 failed due to increased prostate specific antigen, including only 5 with subsequent progression by biopsy criteria. When prostate specific antigen was excluded from progression criteria, only 32 cases progressed, and 2 and 5-year progression-free probability was 91% and 76%, respectively. Using modified criteria as an end point positive confirmatory biopsy was the only independent predictor of progression (HR 3.16, 95% CI 1.41-7.09, p = 0.005).

    CONCLUSIONS:

    Active surveillance is feasible in patients with low risk prostate cancer and most patients show little evidence of progression within 5 years. There is no clear justification for treating patients in whom prostate specific antigen increases above 10 ng/ml in the absence of other indications of tumor progression. Patients considering active surveillance should undergo confirmatory biopsy to better assess the risk of progression.

    Copyright © 2011 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.


    Comment in
    Nat Rev Urol. 2011 Feb;8(2):60.


    PMID: 21167529 [PubMed - indexed for MEDLINE]</p>

    PSA is not a "flag" to rule AS ?
    Hopeful

    This abstract is somehow confusing in regards to the parameters used in the criteria and the conclusion doesn’t explain details of the negative group of patients.

    I wonder how the researchers could use a biopsy to check for cancer progression in confirmed positive patients.
    Would that be by the number of positive cores? Or by the volume of cancer found in the cores?

    My understanding from this study is that researchers are suggesting that PSA is not a "flag" to rule AS. A Low-risk case is then taken into consideration independently of the level of PSA. However, I see the conclusions with a tendency in recommending AS to patients with no indolent type of cancer, which in my opinion may trigger a series of progression unnoticed and delayed treatments.
    Sensitive assays on the two decimal places (0.XX ng/ml) for testing PSA would be not a due choice for this class of low-risk patients.

    Where am I wrong?

    Regards
    VG
  • tarhoosier
    tarhoosier Member Posts: 195 Member

    PSA is not a "flag" to rule AS ?
    Hopeful

    This abstract is somehow confusing in regards to the parameters used in the criteria and the conclusion doesn’t explain details of the negative group of patients.

    I wonder how the researchers could use a biopsy to check for cancer progression in confirmed positive patients.
    Would that be by the number of positive cores? Or by the volume of cancer found in the cores?

    My understanding from this study is that researchers are suggesting that PSA is not a "flag" to rule AS. A Low-risk case is then taken into consideration independently of the level of PSA. However, I see the conclusions with a tendency in recommending AS to patients with no indolent type of cancer, which in my opinion may trigger a series of progression unnoticed and delayed treatments.
    Sensitive assays on the two decimal places (0.XX ng/ml) for testing PSA would be not a due choice for this class of low-risk patients.

    Where am I wrong?

    Regards
    VG

    Surveillance
    Vasco, I understood the citation provided just above your last comment, or at least until I read you comment. What I believe the research is saying is that biopsy factors are more reliable as indicators to suspend or continue AS than is PSA. Even PSA in addition to those biopsy factors provides no significant additional validation. Biopsies can show a change in the G score and a change in the location and volume of tumor. These would be more significant factors than PSA which, as we know, is not cancer dependent.
    PSA alone is not a "flag" to determine the advance of the disease in men following Active Surveillance, at least within the bounds of PSA followed in the study.
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member

    Surveillance
    Vasco, I understood the citation provided just above your last comment, or at least until I read you comment. What I believe the research is saying is that biopsy factors are more reliable as indicators to suspend or continue AS than is PSA. Even PSA in addition to those biopsy factors provides no significant additional validation. Biopsies can show a change in the G score and a change in the location and volume of tumor. These would be more significant factors than PSA which, as we know, is not cancer dependent.
    PSA alone is not a "flag" to determine the advance of the disease in men following Active Surveillance, at least within the bounds of PSA followed in the study.

    Surveillance
    Tarhoosier

    I appreciate very much your reply and I like to learn but the AS “regulations” is not clear to me (even though I was on WW for 6 years).
    Surely a biopsy is more reliable as indicator of aggressiveness as you comment, and cancer found in additional cores on a second biopsy would indicate a “different” diagnosis or a “change” in the status, but that could have been a cause of a “miss” target in the first attempt. Still I do not understand how a confirmed positive case is declared in “progression” using a biopsy for judgment.
    According to Dr. Myers there are rare cases where Gleason grades have progressed to a more aggressive grade (ex: Gr=3 to 4) after a long period of time. However patients have seen their PSA increase between treatments in the same Gleason grade.

    I recall your post at Califvader’s thread “Possible Remission” (http://csn.cancer.org/node/206974), where you considered his Gs 3+3 (6) but not the increase of his PSA, and that strike me because it is a similar situation as that of mine back in 2001. I was a Gs 2+3 (5), recurred after RP but doctors (JH, MSKCC, TH) suggested I had micro-metastases and put me on WW, and they saw with me my PSA increasing slowly along the 6 years and never recommended a salvage treatment.

    What could be the best definition for “Indolent type of Cancer” ?
    I am confused.

    Thanks
    VGama
  • hopeful and optimistic
    hopeful and optimistic Member Posts: 2,339 Member

    Surveillance
    Tarhoosier

    I appreciate very much your reply and I like to learn but the AS “regulations” is not clear to me (even though I was on WW for 6 years).
    Surely a biopsy is more reliable as indicator of aggressiveness as you comment, and cancer found in additional cores on a second biopsy would indicate a “different” diagnosis or a “change” in the status, but that could have been a cause of a “miss” target in the first attempt. Still I do not understand how a confirmed positive case is declared in “progression” using a biopsy for judgment.
    According to Dr. Myers there are rare cases where Gleason grades have progressed to a more aggressive grade (ex: Gr=3 to 4) after a long period of time. However patients have seen their PSA increase between treatments in the same Gleason grade.

    I recall your post at Califvader’s thread “Possible Remission” (http://csn.cancer.org/node/206974), where you considered his Gs 3+3 (6) but not the increase of his PSA, and that strike me because it is a similar situation as that of mine back in 2001. I was a Gs 2+3 (5), recurred after RP but doctors (JH, MSKCC, TH) suggested I had micro-metastases and put me on WW, and they saw with me my PSA increasing slowly along the 6 years and never recommended a salvage treatment.

    What could be the best definition for “Indolent type of Cancer” ?
    I am confused.

    Thanks
    VGama

    Well,
    as I understand, the biopsy is key in determining where a patient stands. The gleason score shows the aggressiveness of the cancer and gives a strong indication how quickly the cancer will spread.

    There is a DRE, PSA, and other markers to measure disease progression such as a PAP, PCA3, PROpsa and other markers http://ajcp.ascpjournals.org/content/supplements/120/Suppl_1/S85.full.pdf

    that try to measure disease prgression, however I don't think any of them do the job. (see the last study citation, below the dotted line, at the end of this post.

    In answer to your speicific question,
    "Surely a biopsy is more reliable as indicator of aggressiveness as you comment, and cancer found in additional cores on a second biopsy would indicate a “different” diagnosis or a “change” in the status, but that could have been a cause of a “miss” target in the first attempt. Still I do not understand how a confirmed positive case is declared in “progression” using a biopsy for judgment"

    The first biopsy can miss an aggressivre cancer, however if a second biopsy shows this, the patient will no longer be eligible for AS, and will need to seek curative treatment. This aggessive gleason may or may not be progressive from the first biopsy, but simply found on the second biopsy.

    Your next question is the million dollar question, and is one that I am struggling with.

    "What could be the best definition for “Indolent type of Cancer”

    We know that indolent type of cancer means not likely to progress, but how do we measure this? Since I just had a third biopsy, am still being treated with Active Surveillance but am scheduled for another biopsy in two years....a very long way to go......I am very interested in determining indicators other than biopsy that will measure progression of my cancer, if any...I am doing research about this, and am grateful for any input to monitor my disease at this point.
    ----------------------------------------------


    BMC Med Genomics. 2010 Mar 16;3:8.

    Molecular sampling of prostate cancer: a dilemma for predicting disease progression.

    Sboner A, Demichelis F, Calza S, Pawitan Y, Setlur SR, Hoshida Y, Perner S, Adami HO, Fall K, Mucci LA, Kantoff PW, Stampfer M, Andersson SO, Varenhorst E, Johansson JE, Gerstein MB, Golub TR, Rubin MA, Andrén O.


    Source

    Department of Pathology and Laboratory Medicine, Weill Cornell Medical Center, New York, NY, USA.


    Abstract

    BACKGROUND:

    Current prostate cancer prognostic models are based on pre-treatment prostate specific antigen (PSA) levels, biopsy Gleason score, and clinical staging but in practice are inadequate to accurately predict disease progression. Hence, we sought to develop a molecular panel for prostate cancer progression by reasoning that molecular profiles might further improve current clinical models.

    METHODS:

    We analyzed a Swedish Watchful Waiting cohort with up to 30 years of clinical follow up using a novel method for gene expression profiling. This cDNA-mediated annealing, selection, ligation, and extension (DASL) method enabled the use of formalin-fixed paraffin-embedded transurethral resection of prostate (TURP) samples taken at the time of the initial diagnosis. We determined the expression profiles of 6100 genes for 281 men divided in two extreme groups: men who died of prostate cancer and men who survived more than 10 years without metastases (lethals and indolents, respectively). Several statistical and machine learning models using clinical and molecular features were evaluated for their ability to distinguish lethal from indolent cases.

    RESULTS:

    Surprisingly, none of the predictive models using molecular profiles significantly improved over models using clinical variables only. Additional computational analysis confirmed that molecular heterogeneity within both the lethal and indolent classes is widespread in prostate cancer as compared to other types of tumors.

    CONCLUSIONS:

    The determination of the molecularly dominant tumor nodule may be limited by sampling at time of initial diagnosis, may not be present at time of initial diagnosis, or may occur as the disease progresses making the development of molecular biomarkers for prostate cancer progression challenging.


    PMID: 20233430 [PubMed - indexed for MEDLINE] PMCID: PMC2855514 Free PMC
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member

    Well,
    as I understand, the biopsy is key in determining where a patient stands. The gleason score shows the aggressiveness of the cancer and gives a strong indication how quickly the cancer will spread.

    There is a DRE, PSA, and other markers to measure disease progression such as a PAP, PCA3, PROpsa and other markers http://ajcp.ascpjournals.org/content/supplements/120/Suppl_1/S85.full.pdf

    that try to measure disease prgression, however I don't think any of them do the job. (see the last study citation, below the dotted line, at the end of this post.

    In answer to your speicific question,
    "Surely a biopsy is more reliable as indicator of aggressiveness as you comment, and cancer found in additional cores on a second biopsy would indicate a “different” diagnosis or a “change” in the status, but that could have been a cause of a “miss” target in the first attempt. Still I do not understand how a confirmed positive case is declared in “progression” using a biopsy for judgment"

    The first biopsy can miss an aggressivre cancer, however if a second biopsy shows this, the patient will no longer be eligible for AS, and will need to seek curative treatment. This aggessive gleason may or may not be progressive from the first biopsy, but simply found on the second biopsy.

    Your next question is the million dollar question, and is one that I am struggling with.

    "What could be the best definition for “Indolent type of Cancer”

    We know that indolent type of cancer means not likely to progress, but how do we measure this? Since I just had a third biopsy, am still being treated with Active Surveillance but am scheduled for another biopsy in two years....a very long way to go......I am very interested in determining indicators other than biopsy that will measure progression of my cancer, if any...I am doing research about this, and am grateful for any input to monitor my disease at this point.
    ----------------------------------------------


    BMC Med Genomics. 2010 Mar 16;3:8.

    Molecular sampling of prostate cancer: a dilemma for predicting disease progression.

    Sboner A, Demichelis F, Calza S, Pawitan Y, Setlur SR, Hoshida Y, Perner S, Adami HO, Fall K, Mucci LA, Kantoff PW, Stampfer M, Andersson SO, Varenhorst E, Johansson JE, Gerstein MB, Golub TR, Rubin MA, Andrén O.


    Source

    Department of Pathology and Laboratory Medicine, Weill Cornell Medical Center, New York, NY, USA.


    Abstract

    BACKGROUND:

    Current prostate cancer prognostic models are based on pre-treatment prostate specific antigen (PSA) levels, biopsy Gleason score, and clinical staging but in practice are inadequate to accurately predict disease progression. Hence, we sought to develop a molecular panel for prostate cancer progression by reasoning that molecular profiles might further improve current clinical models.

    METHODS:

    We analyzed a Swedish Watchful Waiting cohort with up to 30 years of clinical follow up using a novel method for gene expression profiling. This cDNA-mediated annealing, selection, ligation, and extension (DASL) method enabled the use of formalin-fixed paraffin-embedded transurethral resection of prostate (TURP) samples taken at the time of the initial diagnosis. We determined the expression profiles of 6100 genes for 281 men divided in two extreme groups: men who died of prostate cancer and men who survived more than 10 years without metastases (lethals and indolents, respectively). Several statistical and machine learning models using clinical and molecular features were evaluated for their ability to distinguish lethal from indolent cases.

    RESULTS:

    Surprisingly, none of the predictive models using molecular profiles significantly improved over models using clinical variables only. Additional computational analysis confirmed that molecular heterogeneity within both the lethal and indolent classes is widespread in prostate cancer as compared to other types of tumors.

    CONCLUSIONS:

    The determination of the molecularly dominant tumor nodule may be limited by sampling at time of initial diagnosis, may not be present at time of initial diagnosis, or may occur as the disease progresses making the development of molecular biomarkers for prostate cancer progression challenging.


    PMID: 20233430 [PubMed - indexed for MEDLINE] PMCID: PMC2855514 Free PMC

    24 TYPES OF PROSTATE CANCER
    IRA

    Thanks for the “enlightenment”. This abstract on the “…a dilemma for predicting disease progression…” says it all. Progression cannot be based on biopsy on all situations. Probably it can only in few cases.
    Looking anecdotally to the two following examples I would like to idealize the opinion from those “experts” on AS (Dr. Scardino).

    Situations (1); If one guy finds himself with a Gr=3 on the first biopsy with attached PSA=4.0 and then one year later finds from the second biopsy an increase in grade of Gr=4 with attached PSA=8.0 then he may be recommended to stop AS and start a Treatment.
    Situation (2); If a guy finds himself with a Gr=3 on the first biopsy with attached PSA=4.0 and then one year later finds from the second biopsy an equal grade of Gr=3 with attached PSA=8.0 then he may be recommended to CONTINUE AS.

    Surely the situation (2) would alarm doctors in investigating the cause of the spike in PSA before advising on a continued AS. If the increase in PSA has been confirmed not benign related (ex. BPH, prostate manipulation the day before drawing blood; like sex, riding a bike, etc ), then the case would be judged more serious than the AS regulations.

    PSA, as in the old times, is a predictive “flag” for progression but it may be not an important element/item in the INITIAL decision for recommending a patient to follow AS.
    Even if the study you posted has given negative outcomes for the Molecular Sampling, I am a strong believer on the aneuploid DNA ploidy status in grading the cancers better than the visual comparison with the Gleason pattern scale. I do so because of the many varieties of prostate cancers (24 types) which may be screened with markers other than PSA. This alone reinforces the opinion that PSA can be a flag but not an element in the decision.
    (http://online.wsj.com/article/SB10001424052748703279704575334982806405218.html)

    I consider myself a “pudding-head” on the matter and would like to know more.

    Sincerely
    VGama
  • tarhoosier
    tarhoosier Member Posts: 195 Member

    Surveillance
    Tarhoosier

    I appreciate very much your reply and I like to learn but the AS “regulations” is not clear to me (even though I was on WW for 6 years).
    Surely a biopsy is more reliable as indicator of aggressiveness as you comment, and cancer found in additional cores on a second biopsy would indicate a “different” diagnosis or a “change” in the status, but that could have been a cause of a “miss” target in the first attempt. Still I do not understand how a confirmed positive case is declared in “progression” using a biopsy for judgment.
    According to Dr. Myers there are rare cases where Gleason grades have progressed to a more aggressive grade (ex: Gr=3 to 4) after a long period of time. However patients have seen their PSA increase between treatments in the same Gleason grade.

    I recall your post at Califvader’s thread “Possible Remission” (http://csn.cancer.org/node/206974), where you considered his Gs 3+3 (6) but not the increase of his PSA, and that strike me because it is a similar situation as that of mine back in 2001. I was a Gs 2+3 (5), recurred after RP but doctors (JH, MSKCC, TH) suggested I had micro-metastases and put me on WW, and they saw with me my PSA increasing slowly along the 6 years and never recommended a salvage treatment.

    What could be the best definition for “Indolent type of Cancer” ?
    I am confused.

    Thanks
    VGama

    Communication breakdown
    This discussion is another example, if anyone needed such, that online interaction is no substitute for personal direct communication.
    My original response above was to the opening post in the thread about the issue of active surveillance in the case of a man with one core positive out of 31, with less than 5% of G6 cancer. This is a little as possible to detect. The psa change(s) that the initial post author mentioned in another post elsewhere at this site was perhaps the start of some confusion. Nonetheless, there was also a post about the role of biopsy and psa in AS. Biopsy is definitive, and psa is suggestive. To go to PRIMARY treatment on suggestive rather than definitive evidence is wrong. I believe that was the conclusion of the research mentioned in the post by "hopeful". I agree with that conclusion.
    After a biopsy such as that for daveirving at the top of this thread, further biopsies would be in order at some interval such as annual or every two years. The results of these biopsies may show some greater risk with G score advancing, more cores positive, a greater percentage of the cores positive or cancer noted at or near the margin of the gland. Psa would be a less important issue than biopsy factors. Psa may indicate more frequent biopsy or biopsy localized to one area or a change from transrectal to perineal to reach areas not well identified with the other type of biopsy.
    I believe that prostate cancer is a progressive disease and over time will progress from G3 to G4 and eventually G5 if not addressed. I am unaware of the "rare" cases that Myers may have referred to. I think that progression is the standard for the disease. It may happen over such a long time that other health risks may impose themselves prior to the lethal stage. Such may be the case with G3+3 disease.
    In regard to SECONDARY treatment I was most interested in the G score that califvader presented which was 3+3. This is an indicator of the slowest growing prostate cancer and indeed his psa was going DOWN at the time he wrote. This is what I wrote about califvader at that time:
    ******
    Based on the limited information provided by ca.vader he has been watchfully waiting on his psa. His G6 has, as is often the case, allowed a very slow rise. His psa doubling time is impossible to determine, though his most recent psa direction was actually negative, 4.8 to 3.3. If, as I assume, his psa has been moving over some years, then this means that he has some more years to go before addressing ADT. I also assume he is on no therapy at this time. A "threat to his health" would entail symptoms or side effects serious enough to cause further treatment. I believe he is still years away from that.
    It is crystal clear from his post that he is comfortable watching his psa and waiting to address the issue until some later time. Apparently his doctor(s) is (are) as well. I believe this is supported by the (few) facts he presents. I find no reason to encourage him to abandon his current course and to begin a systemic treatment.
    ***********

    Vasco, your situation was post-treatment and not the same one as daveirving, or indeed the research subjects from "hopeful". Yours was a choice to monitor and determine when to intervene with hormone (or radiation). Biopsy was not an issue with you post treatment.
    I hope this clears some confusion about what I believe about the two men discussed, califvader and daveirving, and the research presented
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member

    Communication breakdown
    This discussion is another example, if anyone needed such, that online interaction is no substitute for personal direct communication.
    My original response above was to the opening post in the thread about the issue of active surveillance in the case of a man with one core positive out of 31, with less than 5% of G6 cancer. This is a little as possible to detect. The psa change(s) that the initial post author mentioned in another post elsewhere at this site was perhaps the start of some confusion. Nonetheless, there was also a post about the role of biopsy and psa in AS. Biopsy is definitive, and psa is suggestive. To go to PRIMARY treatment on suggestive rather than definitive evidence is wrong. I believe that was the conclusion of the research mentioned in the post by "hopeful". I agree with that conclusion.
    After a biopsy such as that for daveirving at the top of this thread, further biopsies would be in order at some interval such as annual or every two years. The results of these biopsies may show some greater risk with G score advancing, more cores positive, a greater percentage of the cores positive or cancer noted at or near the margin of the gland. Psa would be a less important issue than biopsy factors. Psa may indicate more frequent biopsy or biopsy localized to one area or a change from transrectal to perineal to reach areas not well identified with the other type of biopsy.
    I believe that prostate cancer is a progressive disease and over time will progress from G3 to G4 and eventually G5 if not addressed. I am unaware of the "rare" cases that Myers may have referred to. I think that progression is the standard for the disease. It may happen over such a long time that other health risks may impose themselves prior to the lethal stage. Such may be the case with G3+3 disease.
    In regard to SECONDARY treatment I was most interested in the G score that califvader presented which was 3+3. This is an indicator of the slowest growing prostate cancer and indeed his psa was going DOWN at the time he wrote. This is what I wrote about califvader at that time:
    ******
    Based on the limited information provided by ca.vader he has been watchfully waiting on his psa. His G6 has, as is often the case, allowed a very slow rise. His psa doubling time is impossible to determine, though his most recent psa direction was actually negative, 4.8 to 3.3. If, as I assume, his psa has been moving over some years, then this means that he has some more years to go before addressing ADT. I also assume he is on no therapy at this time. A "threat to his health" would entail symptoms or side effects serious enough to cause further treatment. I believe he is still years away from that.
    It is crystal clear from his post that he is comfortable watching his psa and waiting to address the issue until some later time. Apparently his doctor(s) is (are) as well. I believe this is supported by the (few) facts he presents. I find no reason to encourage him to abandon his current course and to begin a systemic treatment.
    ***********

    Vasco, your situation was post-treatment and not the same one as daveirving, or indeed the research subjects from "hopeful". Yours was a choice to monitor and determine when to intervene with hormone (or radiation). Biopsy was not an issue with you post treatment.
    I hope this clears some confusion about what I believe about the two men discussed, califvader and daveirving, and the research presented

    Tarhoosier; Thanks
    Tarhoosier

    I appreciate again your insight on the biopsy affair, I like to learn and so being inquisitive on details.
    I absolutely agree that biopsy is the practical way to diagnose cancer and the only way at present days to pinpoint aggressiveness and risks. Nevertheless, PSA deserves some respect too.

    This thread by Dave was in fact not inquiring about AS but about any “missing” information on his biopsy. Dave has previously posted in another thread his cancer chronology indicating a progressive diagnosis in both fronts; biopsy and PSA, which are cautious indicators that the cancer has no indolent characteristics but progressive. (http://csn.cancer.org/node/221127)
    Comments on that thread by survivors may have caused David to inquire details on his latest biopsy results in this thread.

    Active Surveillance is a fascinating modality in the management of prostate cancer and the most advisable way for low risk cases where, in my layman’s opinion, the cancer shows to have indolent characteristics.
    I am a fan of AS but would only suggest that modality in cases where the cancer has “dormant” evolution in terms of upgraded classifications (volume) and PSA.
    This is not the case reported by Dave.

    I have noticed that there is controversy regarding the biopsies taken along AS management, particularly on the subject to classify progression. Many studies have been produced, but many doctors question the value of the upgraded score in proving “progression” because of the many proved cases in which the grades were under-classified in biopsies by pathologists. They have compared samples of the same “flesh” between biopsies cores with those from prostatectomies.

    One study on AS patients has shown that early upgrading was linked to initial sampling error (a miss). Researchers in their conclusion write this;

    “Conclusions;
    Within the first 3 years after diagnosis of Gleason score 6 prostate cancer, there is a relatively low risk of grade progression. Within the first 3 years, our data suggest that in most cases tumor grade did not evolve but rather that the higher grade component was not initially sampled since most grade changes occurred relatively soon after biopsy. Grade progression does appear to occur in some men with long-term followup who had multiple biopsies showing Gleason score 6 followed by higher grade cancer.”

    In my layman’s logic three years is too long to diagnose progress in a “probable” missing case. I would imagine the rise of many unnoticed progressions and consequent delayed treatments, if other markers, such as the PSA, is not used as “flags” and given a role in the judgment process.

    WW (Watchful Waiting) is not the same as AS, but it is similar and it is the predecessor of AS. Biopsy taken from the prostate fossa and lymph nodes may substitute the biopsy from the prostate to evaluate for any upgrade of Gleason; however, it is logical to think that in post-surgery cases (like mine and Califvader’s) who were suggested to WW, the measurement of “progression” should be done with other parameters (which one?).
    PSA is still the most reliable marker to indicate cancer activity. Progression in recurrence RP cases has a set value of PSA=0.20 ng/ml as the threshold to trigger treatment.

    Thanks for the post.
    Wishing you the best.

    VGama

    Note; How well is progressing your ADT.
  • tarhoosier
    tarhoosier Member Posts: 195 Member

    Tarhoosier; Thanks
    Tarhoosier

    I appreciate again your insight on the biopsy affair, I like to learn and so being inquisitive on details.
    I absolutely agree that biopsy is the practical way to diagnose cancer and the only way at present days to pinpoint aggressiveness and risks. Nevertheless, PSA deserves some respect too.

    This thread by Dave was in fact not inquiring about AS but about any “missing” information on his biopsy. Dave has previously posted in another thread his cancer chronology indicating a progressive diagnosis in both fronts; biopsy and PSA, which are cautious indicators that the cancer has no indolent characteristics but progressive. (http://csn.cancer.org/node/221127)
    Comments on that thread by survivors may have caused David to inquire details on his latest biopsy results in this thread.

    Active Surveillance is a fascinating modality in the management of prostate cancer and the most advisable way for low risk cases where, in my layman’s opinion, the cancer shows to have indolent characteristics.
    I am a fan of AS but would only suggest that modality in cases where the cancer has “dormant” evolution in terms of upgraded classifications (volume) and PSA.
    This is not the case reported by Dave.

    I have noticed that there is controversy regarding the biopsies taken along AS management, particularly on the subject to classify progression. Many studies have been produced, but many doctors question the value of the upgraded score in proving “progression” because of the many proved cases in which the grades were under-classified in biopsies by pathologists. They have compared samples of the same “flesh” between biopsies cores with those from prostatectomies.

    One study on AS patients has shown that early upgrading was linked to initial sampling error (a miss). Researchers in their conclusion write this;

    “Conclusions;
    Within the first 3 years after diagnosis of Gleason score 6 prostate cancer, there is a relatively low risk of grade progression. Within the first 3 years, our data suggest that in most cases tumor grade did not evolve but rather that the higher grade component was not initially sampled since most grade changes occurred relatively soon after biopsy. Grade progression does appear to occur in some men with long-term followup who had multiple biopsies showing Gleason score 6 followed by higher grade cancer.”

    In my layman’s logic three years is too long to diagnose progress in a “probable” missing case. I would imagine the rise of many unnoticed progressions and consequent delayed treatments, if other markers, such as the PSA, is not used as “flags” and given a role in the judgment process.

    WW (Watchful Waiting) is not the same as AS, but it is similar and it is the predecessor of AS. Biopsy taken from the prostate fossa and lymph nodes may substitute the biopsy from the prostate to evaluate for any upgrade of Gleason; however, it is logical to think that in post-surgery cases (like mine and Califvader’s) who were suggested to WW, the measurement of “progression” should be done with other parameters (which one?).
    PSA is still the most reliable marker to indicate cancer activity. Progression in recurrence RP cases has a set value of PSA=0.20 ng/ml as the threshold to trigger treatment.

    Thanks for the post.
    Wishing you the best.

    VGama

    Note; How well is progressing your ADT.

    I-ADT
    Restarted ADT-2 December, 2010. PSADt=30Days+/-. psa at that time ~3.5. I reached 0.01 first two times on ADT.
    Current psa 0.08 at seven months of treatment. I am pleased. I take 400 mg Celecoxib Am and again Pm. Bio curcumin also used, plus Vit D. D supplementation @15,000 I. U. / day. I have learned that this is necessary for me. Current D3 reading is 77 ng.
    I saw my primary physician this week and I am ridiculously healthy for a 63-64 y. o. man. I use simvastatin to keep Cholesterol in "ideal" range. Cholesterol figures are satisfactory without it. There is a potential advantage for PCa with low cholesterol in serum so I continue it at low cost by generic drug.
    Thanks for asking and keep posting.
  • mrspjd
    mrspjd Member Posts: 694 Member

    I-ADT
    Restarted ADT-2 December, 2010. PSADt=30Days+/-. psa at that time ~3.5. I reached 0.01 first two times on ADT.
    Current psa 0.08 at seven months of treatment. I am pleased. I take 400 mg Celecoxib Am and again Pm. Bio curcumin also used, plus Vit D. D supplementation @15,000 I. U. / day. I have learned that this is necessary for me. Current D3 reading is 77 ng.
    I saw my primary physician this week and I am ridiculously healthy for a 63-64 y. o. man. I use simvastatin to keep Cholesterol in "ideal" range. Cholesterol figures are satisfactory without it. There is a potential advantage for PCa with low cholesterol in serum so I continue it at low cost by generic drug.
    Thanks for asking and keep posting.

    Tarhoosier Question
    In another thread you previously indicated being on ADT3. Did you discontinue the 5 alpha reductase inhibitor or did you remain on it during ADT2 vacation; hence, the restart of ADT2 (assuming LHRH agonist + bicalutamide)? T and DHT levels measured? Also, taking any bisphosphonates, etc to increase bone mineral density while on ADT? Thanks.

    May you continue to be even more ridiculously healthy. All the best.
  • tarhoosier
    tarhoosier Member Posts: 195 Member
    mrspjd said:

    Tarhoosier Question
    In another thread you previously indicated being on ADT3. Did you discontinue the 5 alpha reductase inhibitor or did you remain on it during ADT2 vacation; hence, the restart of ADT2 (assuming LHRH agonist + bicalutamide)? T and DHT levels measured? Also, taking any bisphosphonates, etc to increase bone mineral density while on ADT? Thanks.

    May you continue to be even more ridiculously healthy. All the best.

    Protocol
    By the management of my oncologist, I have monthly testing. DHT is less than 5, which is the low limit of assay and dutasteride is suspended. I tried using it even with DHT at very low levels and there was no result on psa, as I would have predicted. Save it for later when off treatment. Bisphosphonate is also suspended due to concern over long term use and splinter-fracture. My neighbor is a breast cancer survivor and and multi-year user of Fosamax and she is now a cripple due to catastrophic fractures in both femurs. Riveted my attention, it did. My oncologist prefers low dose estrogen by patch to treat bone density and I have yet to start that. I should ask him about that next visit.
  • hopeful and optimistic
    hopeful and optimistic Member Posts: 2,339 Member

    24 TYPES OF PROSTATE CANCER
    IRA

    Thanks for the “enlightenment”. This abstract on the “…a dilemma for predicting disease progression…” says it all. Progression cannot be based on biopsy on all situations. Probably it can only in few cases.
    Looking anecdotally to the two following examples I would like to idealize the opinion from those “experts” on AS (Dr. Scardino).

    Situations (1); If one guy finds himself with a Gr=3 on the first biopsy with attached PSA=4.0 and then one year later finds from the second biopsy an increase in grade of Gr=4 with attached PSA=8.0 then he may be recommended to stop AS and start a Treatment.
    Situation (2); If a guy finds himself with a Gr=3 on the first biopsy with attached PSA=4.0 and then one year later finds from the second biopsy an equal grade of Gr=3 with attached PSA=8.0 then he may be recommended to CONTINUE AS.

    Surely the situation (2) would alarm doctors in investigating the cause of the spike in PSA before advising on a continued AS. If the increase in PSA has been confirmed not benign related (ex. BPH, prostate manipulation the day before drawing blood; like sex, riding a bike, etc ), then the case would be judged more serious than the AS regulations.

    PSA, as in the old times, is a predictive “flag” for progression but it may be not an important element/item in the INITIAL decision for recommending a patient to follow AS.
    Even if the study you posted has given negative outcomes for the Molecular Sampling, I am a strong believer on the aneuploid DNA ploidy status in grading the cancers better than the visual comparison with the Gleason pattern scale. I do so because of the many varieties of prostate cancers (24 types) which may be screened with markers other than PSA. This alone reinforces the opinion that PSA can be a flag but not an element in the decision.
    (http://online.wsj.com/article/SB10001424052748703279704575334982806405218.html)

    I consider myself a “pudding-head” on the matter and would like to know more.

    Sincerely
    VGama

    Vasco
    My knowledge is limited in measuring the progress of Active Surveillance, and would like to know more. After your comment about DNA Ploidy I reviewed my medical records, and I notice that I did not have a DNA Ploidy at the time of my diagnosis , in MARCH 2009 when I was diagnosed...since then I had two biopsies that have been benign.....plus other indicator tests list in about me .....if I had to do over again with more knowledge, I would have asked for the test.......at this point, I don't know if it would do much for me...what do you think.?

    Below is some info on DNA Ploidy that I took off the internet

    "DNA Ploidy and Prostate Cancer Cells

    One of the many purposes of a prostate biopsy is to perform a DNA Ploidy analysis. A DNA Ploidy analysis assesses the DNA characteristics of prostate cancer cells and may be conducted after a prostate biopsy has been performed. Prostate cancer cells can be classified as diploid, tetraploid, or aneuploid according to the amount of DNA in their nuclei. Cancerous cells that are more similar to normal cells are known as diploid, meaning that the nucleus of the cell contains the appropriate number of human chromosomes. Tetraploid means the nucleus of the cell contains four times as many chromosomes as a healthy cell, while aneuploid contains either too many or too few. Studies have shown that patients with diploid cancers have longer disease-free periods and extended recurrence-free survival times. For this reason DNA Ploidy analysis may be helpful in determining the grade of your cancer. Diploid prostate cancer cells are well-differentiated, or similar to healthy cells, and are more responsive to hormonal therapy than tetraploid or aneuploid cells. Therefore DNA Ploidy analysis may be able to predict how a patient will respond to prostate cancer treatments.

    DNA Ploidy has become a relatively inexpensive and clinically available test. Your physician, through a prostate biopsy or certain prostatectomy procedures using either flow cytometry measurement (FLM) or static image cytometry (SIC), can perform this type of prostate cancer diagnosis. Flow cytometry refers to the measurement of the physical and chemical characteristics of a cell. Static image cytometry is used for clarifying indistinct areas in flow cytometry results. A doctor may order DNA Ploidy analysis if when he or she believes that the analysis will make a difference for the prostate cancer patient’s treatment options. A doctor will be able to determine whether a patient will benefit from a DNA Ploidy test based on his PSA level, Gleason score, and stage of prostate cancer. However, if a doctor has all the information needed to estimate that you have aggressive prostate cancer, then the DNA Ploidy test is unnecessary."


    Vasco, like you I'm interested in knowing more about each of these various measuremtments, and would like to know what (I'm thinking ) the best ones are, and the best combination of these to provide guidance in monitoring the progression of disease in Active surveillance patients.
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member

    Protocol
    By the management of my oncologist, I have monthly testing. DHT is less than 5, which is the low limit of assay and dutasteride is suspended. I tried using it even with DHT at very low levels and there was no result on psa, as I would have predicted. Save it for later when off treatment. Bisphosphonate is also suspended due to concern over long term use and splinter-fracture. My neighbor is a breast cancer survivor and and multi-year user of Fosamax and she is now a cripple due to catastrophic fractures in both femurs. Riveted my attention, it did. My oncologist prefers low dose estrogen by patch to treat bone density and I have yet to start that. I should ask him about that next visit.

    Hopeful; With no regrets HAVE IT DONE
    IRA

    You may laugh on my little story on the subject you question, and so did some of the doctors I met along the journey of my cancer management, but I keep two samples/slides of my prostate in my survivor’s file.
    Back in 2000 after diagnosis and been asked “HAVE YOU decided on a treatment?”, I went bananas and read every paper I could hold on prostate cancer. Since then I become an avid researcher and the subject that most fascinated me at the time was about the role that the Immunotherapy can have in the fight of this bandit. There were many undergoing studies on “vaccines” like therapies but these could be successful if “manufactured” to each particular case. The only way to have it done was through the information stored in the DNA of each one of us. I realised that a piece of my prostate was as important as a copy of the pathological report.

    You can request a DNA test of your prostate using the core samples from the biopsy. Your doctor/hospital/clinic has the samples in their possession. How much that is helpful in your case, is evidenced in the article you posted. The usual aneuploid DNA ploidy status helps to determine probable aggressiveness. Logically one could expect Gleason patterns of 4 and 5 of being associated with aneuploidy cells. To know your P-cell type in your benign case can give you peace of mind for the interval years between biopsies. It wouldn’t surprise me if your P-cells turn to be Tetraploid (Gr=1).

    For the future, the simple DNA test can be helpful in determining on a drug that cold better target the genetic variants in your chromosomes. This seems to be a “very near future” that will help many (including myself), when we read about the several practical successful studies being carried out. Provenge is one offspring product and so it is the latest test result on a vaccine posted here by MrsPJD (http://csn.cancer.org/node/220987).
    It doesn’t “hurt” to have a sample of our flesh and the heredity test (DNA) of cell’s genome filed with the other common data on PCa.

    In Europe much fuzze has been talked since BBC’s announcement of a cheaper DNA test. This will surely facilitate more and more developments on diagnosis, treatments and medicines for combating all types of cancer.

    The best to you.
    VGama
  • hopeful and optimistic
    hopeful and optimistic Member Posts: 2,339 Member

    Hopeful; With no regrets HAVE IT DONE
    IRA

    You may laugh on my little story on the subject you question, and so did some of the doctors I met along the journey of my cancer management, but I keep two samples/slides of my prostate in my survivor’s file.
    Back in 2000 after diagnosis and been asked “HAVE YOU decided on a treatment?”, I went bananas and read every paper I could hold on prostate cancer. Since then I become an avid researcher and the subject that most fascinated me at the time was about the role that the Immunotherapy can have in the fight of this bandit. There were many undergoing studies on “vaccines” like therapies but these could be successful if “manufactured” to each particular case. The only way to have it done was through the information stored in the DNA of each one of us. I realised that a piece of my prostate was as important as a copy of the pathological report.

    You can request a DNA test of your prostate using the core samples from the biopsy. Your doctor/hospital/clinic has the samples in their possession. How much that is helpful in your case, is evidenced in the article you posted. The usual aneuploid DNA ploidy status helps to determine probable aggressiveness. Logically one could expect Gleason patterns of 4 and 5 of being associated with aneuploidy cells. To know your P-cell type in your benign case can give you peace of mind for the interval years between biopsies. It wouldn’t surprise me if your P-cells turn to be Tetraploid (Gr=1).

    For the future, the simple DNA test can be helpful in determining on a drug that cold better target the genetic variants in your chromosomes. This seems to be a “very near future” that will help many (including myself), when we read about the several practical successful studies being carried out. Provenge is one offspring product and so it is the latest test result on a vaccine posted here by MrsPJD (http://csn.cancer.org/node/220987).
    It doesn’t “hurt” to have a sample of our flesh and the heredity test (DNA) of cell’s genome filed with the other common data on PCa.

    In Europe much fuzze has been talked since BBC’s announcement of a cheaper DNA test. This will surely facilitate more and more developments on diagnosis, treatments and medicines for combating all types of cancer.

    The best to you.
    VGama

    VG
    Thanks for your post, and the excellent information that you shared.

    In response to your comment about laughing because you keep a couple of DNA samples.......I am not laughing....instead I am impressed with your brilliance and ability to follow up.

    I am still interested in investigating various tests to be used in an Active Surveillance protocol for delayed treatment.

    I hope to post various investigative technique to determine how effective each one is , and determine which combination of tests is "best" in an active surveillance program.

    I wonder if you, or others can post any combination of protocols that you find that are used at various institutions.