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Medical Forum / Diseases and Disorders / Prostate Cancer / March 2006new ADT research: comments?
http://www.healthcentral.com/newsdetail/408/1507831.html Not exactly the news that I was looking for.  SignaturePSA 16 10/17/2000 @ 46 Biopsy 11/01/2000 G7 (3+4), T2c RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins PSA .1 .1 .1 .27 .37 .75 EBRT 05-07/2002 @ 47 PSA .34 .22 .15 .21 .32 Lupron 07/03 (1 mo) 8/03 (4 mo), 12/03, 4/04, 09/04, 01/05, 5/05, 10/05, 2/06 PSA .07 .05 .06 .09 .08 .132 Non Illegitimi Carborundum > http://www.healthcentral.com/newsdetail/408/1507831.html > Not exactly the news that I was looking for Sorry, Steve. I hesitated to post this,thinking of you and others. But as one who will probably .have to make the decision whether to go on ADT, I'm hoping some responses may help get at the truth, which is what we all want (badly, and bottom line). It puzzles me so much. On ADT the PSA definitely goes down, and surely that is sign that it is working on the PCa. I have a very good oncologist, a teacher and lecturer and researcher, and it is hard for me to believe that he could be so wrong about this. Surely if it is producing a lower PSA it is slowing down the spread, whcih buys time. refently I saw an article that some group is devloping a drug to replace chimotherapy, which shoud be ready fairly soon (I lost the URL to it before I could post it here) and gives at least another three years, by which time it is possible the vaccine being developed may be ready (a vaccine which works on PCa that has already spread--again I lost the URL).. >> http://www.healthcentral.com/newsdetail/408/1507831.html >> Not exactly the news that I was looking for > > Sorry, Steve. I hesitated to post this,thinking of you and others. Never hesitate. It may not be good news, but we all need accurate information. Furthermore, it was merely a snippet compared to, I'm sure, the actual report on the matter. We may find out that all they discovered was that cancer cells spread through the blood stream even while they are dormant. What we really need is for someone who understands such things to pour through the actual report and tell us what it really says. Until then, I think I will trust that all those docs who came up with orchictomy, estrogen, Lupron, etc. They must have had a good reason. > Until then, I think I will trust that all those docs who came up with > orchictomy, estrogen, Lupron, etc. They must have had a good reason. Well, we KNOW what motivates drug companies, and there's nothing inherently wrong with that. But we also know hows estrogen replacement therapy worked out ... and Thalidomide, and many of the antioxidants, and Phen Fen, and silicone, and prescription hay fever meds, and on and on and on. *O*T*O*H* ... Steve Jordan is obviously dead right. Press releases have become as unreliable as what passes for actual news, whether they're about medicine, politics, the latest disappearance of some white chick, or anything else. It's become blatantly obvious that most of the media is concerned FAR less about accuracy, ethics, or the national welfare than about agendas and egos. I.P. Well, Walsh has been saying all along that all ADT does is knock back the androgen-sensitive cell population while the independent one lies in wait. This may be some some support for Ed Friedman's model, which I can't begin to understand or explain in detail, that implies that depriving PCa of what it naturally needs to survive just results in it developing the ability to survive w/o it. I.e. ADT actually promotes androgen independence. Conversely, Ed postulates that high doses of testosterone w/ an antiandrogen (Casodex) may result in increased apoptosis w/o triggering the development of independency. [Ed, I apologize for the oversimplification - feel free to jump in.] Bill Denton RP 2/12/02 PSA .67 Memphis > Well, Walsh has been saying all along that all ADT does is knock back > the androgen-sensitive cell population while the independent one lies > in wait. No surprise. > This may be some some support for Ed Friedman's model, which I > can't begin to understand or explain in detail, that implies that > depriving PCa of what it naturally needs to survive just results in it > developing the ability to survive w/o it. And what is the difference between androgen-dependent and androgen-independent PCa cells, and how does testosterone modulate it? In the same cell population? An implication is insufficient motivation for me to change substantially my tx regimen. > I.e. ADT actually promotes androgen independence. Show me evidence that ADT *promotes* AIPCa (androgen-independent prostate cancer). Hello, Leibowitz? Regards, Steve J "The thing is to expect nothing in particular, but be aware of the lack of enforceable guarantees or enforceable contracts with nature/god/entropy as to the condition or durability of our bodies." -- Brian Brunner, PCa survivor, December 12, 2005 on The Prostate Problems Mailing List Thank you, Brian. ... > Show me evidence that ADT *promotes* AIPCa (androgen-independent prostate cancer). > Hello, Leibowitz? ... As I understand the standard theory, ADT doesn't promote androgen independence at all. It just keeps the dependent tumor cells from multiplying. The independent cells would, presumably, multiply at the same rate whether the patient is on ADT or not. Eventually they dominate not because they grow faster on ADT but because the lack of growth of the dependent cells allows only the independent cells to grow. That's the theory anyway. Twenty or thirty years from now someone will actually have the facts and, who knows, maybe some of us will still be around to hear about them. Alan Alan and Steve J., like I said, this is very complicated and I don't pretend to understand it, but there is significant evidence that ADPCa may mutate into AIPCa. It has to do w/ androgen receptors. That is one reason why Strum et al. think that it is important to kill off as much of the ADPCa as early as possible - fewer cells to mutate. I agree it is way too early to be changing Tx protocols based on a theory as much in its infancy as this one, but thinking outside the box may the way this disease gets licked. Bill Denton RP 2/12/02 PSA .67 Memphis P.S. Coincidentally, see Leonard's post. Bill > there is significant evidence that ADPCa > may mutate into AIPCa. It has to do w/ androgen receptors. That is one > reason why Strum et al. think that it is important to kill off as much > of the ADPCa as early as possible - fewer cells to mutate. The flip side of that coin was minted by a meta-study of the peer-reviewed research (as opposed to Strum's unreviewed publications) of Walsh, Mayo, S-K, the ACS, and several major universities: It found no evidence that early adjuvant ADT provides any advantage, even with rising PSA. The meta-study specifically cited failure to prolong life and accelerated refraction (along with QOL). PC experts Sonny and Cher said it well: "Debate goes on, debate goes on." I.P. > Well, Walsh has been saying all along that all ADT does is knock back > the androgen-sensitive cell population while the independent one lies [quoted text clipped - 11 lines] > PSA .67 > Memphis Bill, Hopefully, my next paper will make things clearer. However, I don't believe that "androgen dependent" PCa actually exists. PCa grows based on its rate of growth R(G). It dies based on its rate of apoptosis R(A). So long as R(G) is greater than R(A), then PCa will thrive. Under ADT, you are selecting those cells that can survive under those conditions (usually those which produce higher levels of bcl-2). There are some cells that will have a R(G) less than R(A) under the conditions of ADT, and those are commonly referred to as "androgen dependent". Once you understand that there are two androgen receptors, then it becomes clear that ADT works by increase R(A) by eliminating calreticulin (made by mAR), thus making the PCa susceptible to calcium overload apoptosis. Any mutation that results in increased levels of bcl-2 will decrease R(A). If R(A) falls below the level of R(G), then you end up with "androgen independent" PCa. Also, the study cited on ADT ignores the fact that ADT followed by T+F results has been shown to be ~5 times more effective than continual ADT. The reason that I believe that T plus Casodex (and maybe plus F) should be very effective is that you maximize the apoptotic proteins produced by mAR while blocking any increase in R(G) due to androgen binding to iAR and minimizing any downregulation of the apoptotic proteins produced by iAR. Paradoxically, it turns out that if you have both mAR and iAR fully functioning, then any treatment that blocks just one of the androgen receptors coupled with T to stimulate the other should be an extremely effective treatment against PCa. Ed > Not exactly the news that I was looking for. One can't always judge by news reports, but what it appears to cast doubt on is the use of hormone therapy as a primary method to treat localized prostate cancer. I'm sure the small minority who advocate such treatment will point out that much depends on just how you go about it, and, while I don't think they are right about the main issue, I do think they would be right to make that point. In any case, you, Steve, are not in that category. You were treated initially for localized prostate cancer by RP, and that was followed by radiation therapy. Those disn't work, which indicates pretty clearly that your cancer wasn't localized to start with. It is pretty well established that hormone therapy can control metastatic prostate cancer, and that how long it works is quite variable. I believe the only serious argument is about when to begin it, and I don't think the current study sheds much light on that. So, you should entirely ignore this. You seem to be still at a fairly early stage, and we all hope and pray, for all our sakes, not only yours, that something approaching a cure for metastatic prostate cancer will appear in the next few year. >> Not exactly the news that I was looking for. > > One can't always judge by news reports, but what it appears to cast doubt > on is the use of hormone therapy as a primary method to treat localized > prostate cancer. <SOUND LOGIC REDACTED> > So, you should entirely ignore this. I knew you'd dump all over this. Thanks for coming through... >>> Not exactly the news that I was looking for. >>> [quoted text clipped - 7 lines] > > I knew you'd dump all over this. Thanks for coming through... Sooooo ... you're deciding a trial is useless because one person says it is? I don't think ANY of this stuff is THAT cut and dried. And how does anyone decide which expert wins a debate without repeating their clinical research or performing or studying a peer-reviewed analysis of it? Just because something came to us through the media doesn't DISPROVE it; it just means we should use it as a pointer or a heads-up to help us find more facts, not treat it as total bull. Each new "finding" is a piece in a huge, ill-defined puzzle, and time and further reading or actual research may reveal the shape and legitimacy of the piece. i.e., I suspect most factoids are tweaks in the picture, neither earth-shaking nor useless. I.P. > Sooooo ... you're deciding a trial is useless because one person says it > is? No, not the trial... not event he report of the trial... maybe not even the synopsis of the report. But, the news article? Yeah, I guess I have decided it was useless. SignaturePSA 16 10/17/2000 @ 46 Biopsy 11/01/2000 G7 (3+4), T2c RRP 12/15/2000 G7 (3+4), T3cN0M0 Neg margins PSA .1 .1 .1 .27 .37 .75 EBRT 05-07/2002 @ 47 PSA .34 .22 .15 .21 .32 Lupron 07/03 (1 mo) 8/03 (4 mo), 12/03, 4/04, 09/04, 01/05, 5/05, 10/05, 2/06 PSA .07 .05 .06 .09 .08 .132 Non Illegitimi Carborundum >> Sooooo ... you're deciding a trial is useless because one person says it >> is? > > No, not the trial... not event he report of the trial... maybe not even the > synopsis of the report. But, the news article? Yeah, I guess I have > decided it was useless. I gotcha; that makes sense. Maybe the research it references will turn out to be useful once it reaches the light of day. I.P. > http://www.healthcentral.com/newsdetail/408/1507831.html My deep suspicion of the reliability of press reports on medical topics is again vindicated. The ASCO presentation on which the report is based is difficult to identify. Using the name of the quoted source, Tomasz Beer, I found on the ASCO site devoted to the 2006 PCa meeting the following abstract, "Predictors of overall (OS) and cancer-specific survival (CSS) in patients with clinically localized prostate cancer treated with primary androgen deprivation therapy: Results from PCOS." The primary author is J. Graff; Beer is listed as one of the authors. It seems to be the source of the press report. Sure enough, the reporter omitted vital information: for example, the 276 men in the study cohort were using ADT as their *primary tx for clinically localized PCa.* The study does not apply to folks such as Steve Kramer and me. It's at: http://www.asco.org/portal/site/ASCO/menuitem.34d60f5624ba07fd506fe310ee37a01d/? vgnextoid=76f8201eb61a7010VgnVCM100000ed730ad1RCRD&vmview=abst_detail_view&confID =42&abstractID=20049 Or, better yet, http://tinyurl.com/nrovv [You're welcome ;-)] I recommend going to primary sources for reliable information whenever possible. Regards, Steve J "What are the facts? Again and again and again -- what are the facts? Shun wishful thinking, ignore divine revelation, forget 'what the stars foretell,' avoid opinion, care not what the neighbors think, never mind the unguessable 'verdict of history' -- what are the facts, and to how many decimal places? You pilot always into an unknown future; facts are your single clue. Get the facts!" --Lazarus Long Thanks. Now I'm glad I posted the message. And a lesson to be learned about reading these news reports. I think I'll get rid of my Google alerts. >> http://www.healthcentral.com/newsdetail/408/1507831.html > [quoted text clipped - 37 lines] > your single clue. Get the facts!" > --Lazarus Long |
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