Hormone dependent cells vs. hormone independent cells

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Jerry L.
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   Posted 12/28/2010 4:08 PM (GMT -7)   
Can doctors tell from a prostate removed at time of surgery what % of cells are hormone dependent vs. non?

Is there any other technology that can tell this info. before going on HT?
Nov. 2009 Dx at Age 44
Dec. 2009 DaVinci Robotic Surgery
Jan. 2010 T3b, Gleason 9
Feb. 2010 Adjuvant Radiation

PSA History:
-----------------
Nov. 2009 4.30
Feb. 2010 <.05
May 2010 <.05
Aug. 2010 <.05
Nov. 2010 <.05

John T
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   Posted 12/28/2010 4:36 PM (GMT -7)   
Not to my knowledge. I believe the only way to tell is to go on HT and if psa drops to .05 and stays there for a period of months then most or all of the cells are dependent. You also have the testestorone levels at casteration levels for this to occur, I believe this is <20.
JT
65 years old, rising psa for 10 years from 4 to 40; 12 biopsies and MRIS all negative. Oct 2009 DXed with G6 <5%. Color Doppler biopsy found 2.5 cm G4+3. Combidex clear. Seeds and IMRT, no side affects and psa .1 at 1.5 years.

BB_Fan
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   Posted 12/28/2010 5:05 PM (GMT -7)   
I thought that you could determine which of the 24 (?) variations of PCa you have and whether it is a very agressive type. I would assume that this translates into hormone resistant.
Dx PCa Dec 2008 at 56, PSA 3.4
Biopsy: T1c, Geason 7 (3+4) - 8 cores, 4 positive, 30% of all 4 cores.
Robotic Surgery March 2009 Hartford Hospital, Dr Wagner
Pathology Report: T2c, Geason 8, organ confined, negitive margins, lymph nodes negitive - tumor volume 9%, nerves spared, no negitive side effects of surgery.
PSA's < .01, .01, .07, .28, .50. HT 5/10. IMRT 9/10.
PSA's post HT .01, < .01

Jerry L.
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   Posted 12/28/2010 5:28 PM (GMT -7)   
Follow up question - Is it the hormone dependent cells learns how to live in time, the hormone independent cells multiply, or both that causes HT to become ineffective?

BB_Fan
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   Posted 12/29/2010 9:58 AM (GMT -7)   
I have heard two conflicting things on this topic. One medical oncologist told me that HT would continue to work on hormone dependent cells. However, there are some amount of hormone independent cells that will keep on growing and at some point comprise the majority of the cancer cells. I have also read that casodex will at some point stop being effective at killing hormone resistent PCa cells and start feeding them.
 
I am not aware of any evidence that indicates that PCa hormone dependent cells will change to hormone resistent cells over time. However, there are many members of this forum that have a much greater knowledge in this area than I.
Dx PCa Dec 2008 at 56, PSA 3.4
Biopsy: T1c, Geason 7 (3+4) - 8 cores, 4 positive, 30% of all 4 cores.
Robotic Surgery March 2009 Hartford Hospital, Dr Wagner
Pathology Report: T2c, Geason 8, organ confined, negitive margins, lymph nodes negitive - tumor volume 9%, nerves spared, no negitive side effects of surgery.
PSA's < .01, .01, .07, .28, .50. HT 5/10. IMRT 9/10.
PSA's post HT .01, < .01

John T
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Date Joined Nov 2008
Total Posts : 3769
   Posted 12/29/2010 11:20 AM (GMT -7)   
I believe that about 30% of all advanced PC is compsoed of primarily of dependent cells. That's why approximately 30% of patients given HT will oly go through one course of it and never have psa rise again. The rest is a mixture of dependent and independent cells and depending on the proportion will determine how long HT is effective. There is reason to believe that if HT is started early enough while the independent cells are low in number and they have not yet mutated and built up a resistance to HT that HT may also kill these.
JT
65 years old, rising psa for 10 years from 4 to 40; 12 biopsies and MRIS all negative. Oct 2009 DXed with G6 <5%. Color Doppler biopsy found 2.5 cm G4+3. Combidex clear. Seeds and IMRT, no side affects and psa .1 at 1.5 years.

zufus
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Date Joined Dec 2008
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   Posted 12/29/2010 1:39 PM (GMT -7)   
Jerry's question:
 Can doctors tell from a prostate removed at time of surgery what % of cells are hormone dependent vs. non?

Is there any other technology that can tell this info. before going on HT?
 
Jerry-
A Healingwell- (H_LL No)! They cannot tell such things, even with sampling.  However evidence leading to knowing how aggressive a PCa might be is somewhat useful in determining the pathology DNA ploidy testings  (which is optional and most people don't have it done-go figure). There are 3 types and the first type is closest to normal cells and respond best to hormone therapies it is called  Diploid  (DNA- in pairs like normal cells). The third one is the worst of the 3 and is more resistant to hormone therapies  (as mentioned by Dr. Strum along the way to answering us on P2P and such...he believes in the usefulness of ploidy testings...the rest of the world seems to wear bi-focals on that-LOL). 
 
BB- mentioned the 24 variant types of PCa now that are known about, this is newer news and most docs probably have no clue there is that many types, let alone what is your particular version...pathology guys would hopefully know that and that is art and not pure science. So some people are probably given the correct data, majority of  people likely have the version we normally see...my guess.
 
Just to add something to what John T has already mentioned, it is known that some drugs like estrogenics can cause direct apoptosis on PCa cells (kill them directly) and even on hormone resistant cells (hrpca), may not kill them all.....my doc whom studies all this and keeps current and leads PCa support group on his own doing...has a concept that the PCa 'stem' cells survive and keep the cycle going on and on, no matter what drug therapies are used...this seems maybe to be an answer.  There are some patients whom on estrogenics even with uncureable PCa, managed to live either a long while or just on and on, like Dr. Lee at 27 yrs. worth of PCa (uncureable version).  There were some patients before the PSA era that used such and lived a long time and PCa did not cause their demise. (you have to search for that kind of info...seems all the old school information is missing these days??)

Casey59
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   Posted 12/29/2010 1:42 PM (GMT -7)   

Jerry, regarding questions on treatment of advanced PC, this commonly heard reminder should be re-issued:  one size does not fit all. 

Individualized treatment plans will depend largely on the answers to questions which help characterize the biology of the individual case.  What are the site(s) of metastasis?  What was/is response to prior and current treatments?  What are the testosterone and PSA levels?  Is PSA progression the only evidence of therapy failure, or are there other symptoms?  Is the case androgen-independent (AIPC, which implies the potential for responding to a secondary hormone measure) or hormone-resistant (HRPC, patients who do not respond to various hormone treatments or who have progressed following these treatments and would not be expected to respond to another)?  So, the optimal treatment plan for each case will vary...this is important to keep in mind.

 

To try to address your specific question more directly...

Jerry L. said...
Follow up question - Is it the hormone dependent cells learns how to live in time, the hormone independent cells multiply, or both that causes HT to become ineffective?

I assume that this question is just for your own personal interest and curiosity since one cannot affect this, but here’s a copy/paste of a recent (2009) abstract which I believe addresses the question:

Molecular biology of androgen-independent prostate cancer: the role of the androgen receptor pathway.

Abstract

Prostate cancer (PC) cells express the androgen receptor (AR) and need the presence of androgens to survive. Androgen suppression is the gold standard first-line therapy for metastatic disease. Almost all PC patients initially respond to hormonal therapy, but most of them gradually develop resistance to castration. There is evidence that these tumours that are considered castration-resistant continue to depend on AR signaling. Several mechanisms that enhance AR signaling in an androgen-depleted environment have been elucidated: (1) AR mutations that allow activation by low androgen levels or by other endogenous steroids, (2) AR amplification and/or overexpression, (3) increased local intracrine synthesis of androgens, (4) changes in AR cofactors and (5) cross-talk with cytokines and growth factors. Today, there are a number of novel agents targeting the AR signalling pathway under development, including more effective antiandrogens; inhibitors of CYP17, inhibitors of HSP90, inhibitors of histone deacetylases and inhibitors of tyrosine kinase inhibitors.  

   

Reference:  http://www.ncbi.nlm.nih.gov/pubmed/19155198, or http://www.springerlink.com/content/a275n01140k0261p/fulltext.pdf   (challenging to read)

 

So, in other words, this report says there are several theories on how it happens, but no complete, 100% certainty.

 

 

 


 

Post Edited (Casey59) : 12/29/2010 2:41:32 PM (GMT-7)


Tony Crispino
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Date Joined Dec 2006
Total Posts : 7755
   Posted 12/29/2010 2:47 PM (GMT -7)   
There seems to be a feeling here that hormone dependent versus hormone independent prostate cancer is determined at the onset of prostate cancer. "We all have hormone independent cells that eventually grow large enough to be troublesome"

I don't necessarily agree with this. It is my understanding that this is theory. While it may be partially true, I have also heard that hormone dependent prostate cancer can later become hormone independent. We do not have anyway of establishing what makes all prostate cancers become independent of hormones. If we did we may be able to decipher when some prostate cancers are aggressive versus indolent but there is no science that can provide us definitive proof.

What I have seen as a layman is those cases like this one that i have mentioned before. A 53 year old man having an RP with orchiectomy in 1981. Gleason unknown. 29 years later he has Gleason 10 invasion in his bladder. I think it is not reasonable to assume that he had some hormonally resistant Gleason 10 prostate cancer for so long. It is more reasonable to assume that he did have residual disease that eventually "morphed" into the more aggressive form of the disease.

I am certain that many can pull up opinions that vary, but for me I the likelihood of someone surviving for 29 years with aggressive G10 hormonally resistant prostate cancer is extremely nil. If even possible. I believe that Gleason can change, and I believe that resistance can as well.

So to answer the question? If we ever develop such a test to see what percentage of HRPC exists in a RP specimen, if even 0% was discovered, it does not mean that it won't change.

Tony
Disease:
Advanced Prostate Cancer at age 44 (I am 48 now)
pT3b,N0,Mx (original PSA was 19.8) EPE, PM, SVI. Gleason 4+3=7

Treatments:
RALP ~ 2/17/2007 at the City of Hope near Los Angeles.
Adjuvant Radiation Therapy ~ IMRT Completed 8/07
Adjuvant Hormone Therapy ~ 28 months on Casodex and Lupron.

Status:
"I beat up this disease and took its lunch money! I am in remission."
I am currently not being treated, but I do have regular oncology visits.
I am the president of an UsTOO chapter in Las Vegas

Blog : www.caringbridge.org/visit/tonycrispino

Sancarlos
Regular Member


Date Joined Feb 2010
Total Posts : 242
   Posted 12/29/2010 5:06 PM (GMT -7)   
I have a related question that hopefully one of our experts can answer.

If one has had curative treatment such as seeds and IMRT and is on HT because the cancer was very aggressive, how do we correlate PSA with PSA for someone who does not go on HT. This is a question that obviously pertains to my case and I have simply not been able to get a good answer. Sure would appreciate it if someone could direct me to some relevant literature on this issue. My PSA has dropped to a fairly low number (0.013) and may be still going down, but how meaningful is the number given that I have been on HT for over a year.

Sancarlos
Age 66, PC diagnosed 7/2009 at age 65
Stage: T2c, Gleason: 9 (4 + 5), 6 of 6 cores positive
Bone, CAT and MIR scans negative

Treatment: brachytherapy (103 palladium), 100 gy, 11/2009 + ADT3 (Lupron + Casodex+Avodart) + IMRT on Novalis, 45 gy, 3/2010.

PSA: 7/2009, At time of diagnosis -- 11.9
10/2009 -- 5.0
12/2009 -- 0.56
5/2010 -- 0.15
8/9/2010 -- 0.06
11/2010 -- 0.013

Purgatory
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Date Joined Oct 2008
Total Posts : 24397
   Posted 12/29/2010 5:16 PM (GMT -7)   
Tony, I too, believe that an aggressive strand of PC can morph over time and increase the Gleason level all the way to a 10.

I would have to see the facts of the case, but I could not compehend anyone with a Gleason 10 lasting 29 years, while being in a constant Gleason 10 condition. Doesn't seem like that would be medically possible.

David in SC
Age: 58, 56 dx, PSA: 7/07 5.8, 10/08 16.3
3rd Biopsy: 9/08 7 of 7 Positive, 40-90%, Gleason 4+3
open RP: 11/08, on catheters for 101 days
Path Rpt: Gleason 3+4, pT2c, 42g, 20% cancer, 1 pos marg
Incont & ED: None
Post Surgery PSA: 2/09 .05,5/09 .1, 6/09 .11. 8/09 .16
Post SRT PSA: 1/10 .12, 4/8 .04, 8/6 .06 11/10 Not taking it
Latest: 6 Corr Surgeries to Bladder Neck, SP Catheter since 10/1/9, SRT 39 Sess/72 gy ended 11/09, 21 Catheters, Ileal Conduit Surgery 9/23/10

Casey59
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Date Joined Sep 2009
Total Posts : 3172
   Posted 12/29/2010 7:01 PM (GMT -7)   
Sancarlos said...
I have a related question that hopefully one of our experts can answer.

If one has had curative treatment such as seeds and IMRT and is on HT because the cancer was very aggressive, how do we correlate PSA with PSA for someone who does not go on HT...

 

Sancarlos, I’m no expert but I’ll attempt to give an informative answer.  I should also say that I am not a doctor…if I don’t say it every once in a while, someone else jumps in to remind me.

 

Saying that one is “on HT” can mean multiple things.  Most commonly in advanced PC cases, going “on HT” means a double- or triple-blockade approach in which the goal is to reduce the PSA as low as possible…in fact, down to an ultra-sensitive PSA test level of undetectable (or around 0.05ng/mL) and keep it there as long as possible (and hope it stays low for 12 months or more after going “off” the blockade).  A very low nadir, held for a long time, yields the best prognosis.

 

The information you provided isn't crystal clear, but from what you wrote I think you have been prescribed a single adjuvant HT component to supplement your radiation treatments; probably finasteride...this is a different case than described in the paragraph above.  Finasteride (Proscar) or dutasteride (Avodart) are often given for prostate enlargement, or as part of an adjuvant HT regimen.  These drugs prevent the conversion of testosterone to dihydrotestosterone.  The theoretical basis for using finasteride to prevent PC is that almost all PC cells are responsive to male hormones (androgens).  Because androgens might stimulate the change of normal prostate cells into PC cells and stimulate the growth of PC after they have become malignant, then, the argument goes, if finasteride (or dutasteride) can slow or prevent the production of dyhydrotestosterone, they might slow or prevent the development and progression of PC.

 

The PSA levels in men taking finasteride alone usually decrease by 30% to 70% after about one year.  Perhaps you’ve already heard the general rule of thumb about the need to “re-baseline” one’s PSA by 50% if taking finasteride, and I suspect this was the root of your question.

 

Does this answer your question?


Jerry L.
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   Posted 12/29/2010 7:09 PM (GMT -7)   
Tony,

I assume the 29 year survivor was on HT after his RP. Do you know when he started and the specifics about his HT history?

Post Edited (Jerry L.) : 12/29/2010 6:19:10 PM (GMT-7)


Casey59
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Date Joined Sep 2009
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   Posted 12/29/2010 7:43 PM (GMT -7)   
TC-LasVegas said...
What I have seen as a layman is those cases like this one that i have mentioned before. A 53 year old man having an RP with orchiectomy in 1981. Gleason unknown. 29 years later he has Gleason 10 invasion in his bladder. Tony
 
Tony, I, too, was a bit baffled by how you described this case; although, I suspect it might have been imprecisely conveyed to you and you are simply passing on what you heard.  But if not, then I'm open to new understanding.
 
Your friend had a radical prostatectomy (RP) and orchiectomy in 1981.  In 1981, Gleason scoring was, I guess, less ubiquitous than today, and so it was then "unknown". 
 
Over time, apparently, your friend's PC metastasized to his bladder.  This is where I get lost, because you report this as a "Gleason 10 invasion in his bladder."  My understanding is that Gleason grading is done only to prostate tissues found in either a prostate biopsy or RP specimens...but specifically not of metastasized PC cells in other organs.  If your friend reported to you Gleason 10 cells in is bladder, this would be the first time I've heard of such a thing...but like I said, I'm open to new understanding.
 
Can you please clarify?  Just trying to see if there is something new to learn here.  thanks
 

Jerry L.
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   Posted 12/29/2010 8:05 PM (GMT -7)   
David said...
I would have to see the facts of the case, but I could not compehend anyone with a Gleason 10 lasting 29 years, while being in a constant Gleason 10 condition. Doesn't seem like that would be medically possible.

 
Our friend, Will , is half way there.  16+ years and started with a Gleason 9. 
 

Piano
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Date Joined Apr 2008
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   Posted 12/29/2010 9:30 PM (GMT -7)   
Casey59 said...
Over time, apparently, your friend's PC metastasized to his bladder. This is where I get lost, because you report this as a "Gleason 10 invasion in his bladder." My understanding is that Gleason grading is done only to prostate tissues found in either a prostate biopsy or RP specimens...but specifically not of metastasized PC cells in other organs. If your friend reported to you Gleason 10 cells in is bladder, this would be the first time I've heard of such a thing...but like I said, I'm open to new understanding.
I agree it does sound unusual. But I think in such cases there could be a biopsy or surgery, and since the cancer is still PCa, the grading could have arisen from that.

Fairwind
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Date Joined Jul 2010
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   Posted 12/29/2010 11:58 PM (GMT -7)   
Walsh talks about this in his book..20,30 years ago doctors believed PC became hormone refractory over time..They thought all the cells developed the ability to reproduce without testosterone ..Then himself and others at Johns-Hopkins developed the theory that in any given patient, a certain percentage of PC cells were hormone refractory from the get go, they simply did not need "T" to grow. Most PC cells are very dependent on "T" to grow and divide and without it, they die, leaving the refractory cell that were always there to continue their deadly work..It seems the higher the Gleason score, the more independent the cells become..

If they could figure out exactly how this works, they could cure this disease..

Approximately 10% of PC victims with stage 4 (metastasized) disease live longer than 10 years.. 10% succumb within one year...The rest fall in between..
Age 68.
PSA at age 55: 3.5, DRE normal. Advice, "Keep an eye on it".
age 58: 4.5
" 61: 5.2
" 64: 7.5, DRE "Abnormal"
" 65: 8.5, " normal", biopsy, 12 core, negative...
" 66 9.0 "normal", 2ed biopsy, negative, BPH, Proscar
" 67 4.5 DRE "normal"
" 68 7.0 third biopsy positive, 4 out of 12, G-6,7, 9
RRP Sept 3 2010, pos margin, one pos vesicle nodes neg. Post Op PSA 0.9 SRT, HT, Dec

zufus
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Date Joined Dec 2008
Total Posts : 3149
   Posted 12/30/2010 7:31 AM (GMT -7)   
Mark Moyad just made this statement in the Paact Newsletter page 2 top middle right paragraph. 'Tumors make their own testostorone despite men having castrate levels of 'T' from LHRH drugs and now there is a drug to keep certain tumors from feeding itself so to speak!' (talking about Abiraterone as to this drug).

I have not heard this before that tumors could make their own 'T' or perhaps version of a 'T' as to being fed????? Anybody have other references to such??? We understand about things being able to morph and DNA ploidy anaylsis has been shown to change or be at different levels, even in comparatively same stats looking patients.

This area is the multi-million dollar questions! I would presume.
Dx-2002 total urinary blockage, bPsa 46.6 12/12 biopsies all loaded 75-95% vol.; Gleasons scores 7,8,9's (2-sets), gland size 35, ct and bone scans look clear- ADT3 5 months prior to radiations neutron/photon 2-machines, cont'd. ADT3, quit after 2 yrs. switched to DES 1-mg, off 1+ yr., controlled well, resumed, used intermittently, resumed useage

Sancarlos
Regular Member


Date Joined Feb 2010
Total Posts : 242
   Posted 12/30/2010 8:33 AM (GMT -7)   
Casey

Thank you for your reply.

First, a clarification as to what HT means for me. I was originally put on Lupron as a sole agent, but that was changed to ATD3 (Lupron, Casodex + Avodart) some months ago.

My question was, given that I have had curative treatment and am on ATD3, how do I relate my current PSA to" if I were not on ADT3." In other words, if I went off it tomorrow by what factor would it be expected to rise, say in six months. Are you saying that I should expect to adjust to a new baseline of 50% of the present value?

Sancarlos
Age 66, PC diagnosed 7/2009 at age 65
Stage: T2c, Gleason: 9 (4 + 5), 6 of 6 cores positive
Bone, CAT and MIR scans negative

Treatment: brachytherapy (103 palladium), 100 gy, 11/2009 + ADT3 (Lupron + Casodex+Avodart) + IMRT on Novalis, 45 gy, 3/2010.

PSA: 7/2009, At time of diagnosis -- 11.9
10/2009 -- 5.0
12/2009 -- 0.56
5/2010 -- 0.15
8/9/2010 -- 0.06
11/2010 -- 0.013

zufus
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Date Joined Dec 2008
Total Posts : 3149
   Posted 12/30/2010 8:50 AM (GMT -7)   
San- I have been there and done that and went off all drugs for 1 year as my own test and done intermittent useage with DES (2005) after 2 ys. of ADT3 (2002-2004) and I had worse overall stats than you have. Done pretty well considering my starting points. One way to know is eventually go off drugs and get psa tests done monthly (as I did such to see what and when and velocities). This can tell you a thing or two about how aggressive it might actually be...of course would be at your own risk or done with doctors blessings.

This is the Twilight Zone of PCa....where does one stand in this limbo land? It varies alot and from patient to patient. I doubt your psa would rise all that much in one year is my s.w.a.g. estimate.
Dx-2002 total urinary blockage, bPsa 46.6 12/12 biopsies all loaded 75-95% vol.; Gleasons scores 7,8,9's (2-sets), gland size 35, ct and bone scans look clear- ADT3 5 months prior to radiations neutron/photon 2-machines, cont'd. ADT3, quit after 2 yrs. switched to DES 1-mg, off 1+ yr., controlled well, resumed, used intermittently, resumed useage

tarhoosier
Regular Member


Date Joined Mar 2010
Total Posts : 356
   Posted 12/30/2010 9:39 AM (GMT -7)   
Jerry:
Not exactly the answer to your question, but the percentage of G 4 and G5 and the DNA ploidy of the cell nuclei samples determined to be aneuploid will, together, give a reliable estimate of the aggression of the tumor. A man with G3 diploid cells will remain sensitive to ADT far longer than another man with aneuploid G5. I will post a link which vividly and visually displays the intracrine (within the cell) hormone axis which adds to the castrate resistant tumor growth

tarhoosier
Regular Member


Date Joined Mar 2010
Total Posts : 356
   Posted 12/30/2010 9:42 AM (GMT -7)   
http://advancedprostatecancer.net/

Click on the "understanding CRPC " link for the video. This video is produced by the J & J subsidiary responsible for commercialising Abiraterone.

Casey59
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Date Joined Sep 2009
Total Posts : 3172
   Posted 12/30/2010 10:03 AM (GMT -7)   

Hi again, Sancarlos.

After a quick reminder that I’m no expert, I think that the real answer to your question is:  the game has changed (now that you are “on” ADT3), and so it (relating your “on” PSA test result to an “off” result) doesn’t really matter.  Allow me to explain what I mean.

First of all, you have a challenging case.  Gleason-9, six-of-six cores positive.  No signs of metastasis to your bones (or elsewhere, but most commonly (70%) bones), which is great, but your doctor will undoubtedly watch this closely over the upcoming years while taking proactive steps (via ADT3) to keep it that way…but you are at higher risk than most typical PC patients of this happening somewhere down the road.

The goal of your triple-blockade is to cut-off the sources which feed prostate cancer, and to do so for as long possible because (as discussed earlier in this thread) the cancer will otherwise (most likely) eventually become hormone-resistant.  Many men have been very successful on ADT3, and more specifically on the “intermittent” IADT3 for many years…especially those men who also embrace serious lifestyle modification in the areas of diet, exercise and stress reduction...other sources which also "feed" your prostate cancer.  Dr. Charles “Snuffy” Myers is one of the leading experts in this area, if you wanted to research more.

So, you want to beat-down your PSA (which is the marker for disease progression).  This chart (click on this IMAGE) is in Dr Stephen Strum’s publications (online, and I think also in his book), and shows visually the “Treatment Roadmap” of what you are trying to accomplish on ADT3.  (a) Knock down the PSA by starting ADT3, (b) hold it down for a while on ADT3, (c) typically stop ADT3 and monitor how long the PSA stays down, (d) eventually watch it slowly rise, and then (e) when it crosses a threshold (5 ng/mL shown on the Strum chart, but more recently I’ve heard of 10 ng/mL) restart (“intermittent”) ADT3 again to repeat the cycle.  Here’s a PCRI article from Strum; it’s from 2000, but still good.  LINK

I’m going to politely disagree with zufus’ characterization of this being a “twilight zone” or “limbo land”…I think it typically follows a relatively predictable pattern (shown in the Strum chart), with some natural variation in the un-labeled x-axis (time).

My point here for you Sancarlos, which I hope is now more clear, is that it really doesn’t matter what your PSA might be without ADT3…what matters is if and when it rises after stopping ADT3 (the ADT3 "Treatment Roadmap").

I hope this helps.  I undoubtedly covered some points in this topic which you were already familiar with, but did so in hopes that others less familiar with your type of case might also benefit & learn from reading this post in the future.

 



Sancarlos
Regular Member


Date Joined Feb 2010
Total Posts : 242
   Posted 12/30/2010 10:36 AM (GMT -7)   
Hi Casey,

Thank you for your very informative and interesting answer to my question.

I had also rather assumed that the PSA for my situation at this time would not matter all that much, at least so long as it was not increasing but you have supplied some information that make it easier to understand.

Have a Wonderful New Year.

Sancarlos
Age 66, PC diagnosed 7/2009 at age 65
Stage: T2c, Gleason: 9 (4 + 5), 6 of 6 cores positive
Bone, CAT and MIR scans negative

Treatment: brachytherapy (103 palladium), 100 gy, 11/2009 + ADT3 (Lupron + Casodex+Avodart) + IMRT on Novalis, 45 gy, 3/2010.

PSA: 7/2009, At time of diagnosis -- 11.9
10/2009 -- 5.0
12/2009 -- 0.56
5/2010 -- 0.15
8/9/2010 -- 0.06
11/2010 -- 0.013

BB_Fan
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Date Joined Jan 2010
Total Posts : 977
   Posted 12/30/2010 11:18 AM (GMT -7)   
This is a great tread. Very informative.
Dx PCa Dec 2008 at 56, PSA 3.4
Biopsy: T1c, Geason 7 (3+4) - 8 cores, 4 positive, 30% of all 4 cores.
Robotic Surgery March 2009 Hartford Hospital, Dr Wagner
Pathology Report: T2c, Geason 8, organ confined, negitive margins, lymph nodes negitive - tumor volume 9%, nerves spared, no negitive side effects of surgery.
PSA's < .01, .01, .07, .28, .50. HT 5/10. IMRT 9/10.
PSA's post HT .01, < .01
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