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PSA rising, again!

dwgifford
Posts: 4
Joined: Jun 2008

57 year old - diagnosed in 2001 w/psa of 6, surgery in May 2001, cancer free until October 2007. My psa started to rise in October 2007 and went on hormone therapy in June 2008 when psa was about 8. Had Zolodex shot (3 month) in June, September and Dec. 2008. Started IMRT radiation treatments in October 2008 and completed on Dec. 22, 2008. Psa was about 0.
March 2009 psa started to climb again. Biggest problem is how fast mine doubles. It was doubling every two weeks (not every 10 months)so went to new specialist who put me back on the Zolodex & Casodex in September 2009. Psa went down to 8, was 26, and hovered there for a while. New psa in December shows 11 and rising again. I have an appointment tomorrow and am afraid that I am no longer responding to hormone deprivation treatments and wonder what they will say now? I am not ready to face the possibility of losing this fight but may have to unless another method of treatment shows promise. Chemo sounds like a waste of time if it only gives you a couple of months to live. Am I being selfish? What have others experienced with this issue? Thanks.

William Parkinson
Posts: 60
Joined: Oct 2009

I am so sorry to hear about what is happening to you. It is always shocking to hear of cases where so long after definitive local treatment the treatment ultimately fails. I wanted to tell you about several things you can do which hopefully will help in your situation. First, it might prove useful to have your physician give you the CellSearchTM blood test, which looks for circulating tumor cells. In many cancers, tumor cells are released and this is very true in both prostate and breast cancer. In fact, according to a University of Washington study, something like 57% of men have circulating tumor cells at the time of surgery. What this test can show is whether you have these cells, which I am sure you have, but also it can predict if your in real trouble or not. If my memory serves, something like greater than 5 tumor cells per 750 ml of blood (or some such figure) predicts for tough times ahead. Also, I would search sites like Memorial Sloan-Kettering (NY), Dana-Farber (Boston), Fred Hutchison (Seattle), MD Anderson (Houston) and other prominent cancer centers for clinical trials for patients in your situation. An interesting one was announced recently and I wrote about it not long ago. Scroll down and look for something that says 'New clinical trial....'. If you can join some clinical trial it might just prove very useful for you to extend your life. In the meantime, I would also go on a low glycemic diet. For most cancers, but not ordinarily prostate cancers, the cancer grows so fast that new growth of vascular elements to supply blood to the growing tumor can't keep up with the growth of the neoplasm. Ordinarily, cells prefer to use an energetic pathway called oxidative phosphorylation, which requires oxygen. Since the growth of the cancer cells outstrips the blood supply, and hence oxygen which erythrocytes carry (red blood cells), cancer cells turn to anaerobic glycolysis. This pathway does not need oxygen to work, but it does use lots of glucose. In a case like yours, where the PSA doubling time suggests a fast growing cancer, it would not hurt you at all to switch to a low glucose-low carb diet for now, in an effort to slow down the cancer. In addition, I would not take in large amounts of protein at one time. What happens is that with a large influx of protein or carbohydrates the body produces insulin growth factors, which spur the growth of cancer cells. Also, in a study done at UCLA the use of 8oz of pure pomegranate juice per day slowed PSA doubling time of patients who suffered biochemical recurrence from an average of 12 months to an average of 54 months. Again, it can't hurt to try this in a further effort to slow down the cancer. Furthermore, Epigallocatechin-3-gallate, which is found in green tea, can slightly inhibit the production of vascular growth factor and certain prostate cancer cell lines. I will add some references to support this. Another possibility is to go on sirolimus (known also as rapamycin and sold as Rapamune I think, but there are generics for it). This drug inhibits cell growth and cellular turnover in general (it inhibits a pathway called mTOR, mammalian target of rapamycin, which is responsible for cellular turnover). It halts cells from undergoing complete mitosis (cell division). It has proven effective against both hormone-dependant and hormone-independent prostate cancers. It will not cure your cancer, but it can slow it down. It does have some side effects (including immune suppression), but these can normally be managed and in any case, if you are really in the fight for your life, the side effects will not be worth even worrying about. I will also add some references for you to look at (only a few, since both rapamycin and EGCG have numerous research papers). I am hoping that some type of synergistic effect can be produced, which will slow down the progression of your cancer. If you can, let me know if you had positive surgical margins, seminal vesicle invasion, or extra capsular extensions, at the time of your prostatectomy. These can all make a man more liable to biochemical failure. I hope this helps you.
Cheers
Bill

Green Tea: Epigallocatechin-3-gallate (EGCG) inhibits PC-3 prostate cancer cell proliferation via MEK-independent ERK1/2 activation
Chemico-Biological Interactions
Volume 171, Issue 1, 10 January 2008, Pages 89-95
Daniel S. Albrechta, Elizabeth A. Clubbsa, Mario Ferruzzib and Joshua A. Bomsera

Prostate carcinoma and green tea: (-)epigallocatechin-3-gallate inhibits inflammation-triggered MMP-2 activation and invasion in murine TRAMP model. Sartor L, Pezzato E, Donà M, Dell'Aica I, Calabrese F, Morini M, Albini A, Garbisa S. Int J Cancer. 2004 Dec 10;112(5):823-9.

Green tea catechins suppress the DNA synthesis marker MCM7 in the TRAMP model of prostate cancer. McCarthy S, Caporali A, Enkemann S, Scaltriti M, Eschrich S, Davalli P, Corti A, Lee A, Sung J, Yeatman TJ, Bettuzzi S. Mol Oncol. 2007 Sep;1(2):196-204

Tea beverage in chemoprevention of prostate cancer: a mini-review. Saleem M, Adhami VM, Siddiqui IA, Mukhtar H. Nutr Cancer. 2003;47(1):13-23

Effects of interactions of EGCG and Cd(2+) on the growth of PC-3 cells and their mechanisms. Yu HN, Shen SR, Yin JJ. Food Chem Toxicol. 2007 Feb;45(2):244-9. Epub 2006 Aug 3

Rapamycin: "Inhibition of Tumor Growth Progression by Antiandrogens and mTOR Inhibitor in a Pten-Deficient Mouse Model of Prostate Cancer" Weisheng Zhang1, Joe Zhu1, Clay L. Efferson2, Chris Ware3, Jennifer Tammam2, Minilik Angagaw4, Jason Laskey2, Kimberly A. Bettano1, Shailaja Kasibhatla2, John F. Reilly3, Cyrille Sur5 and Pradip K. Majumder2 Cancer Res 2009;69(18):7466–72.

Pilot study of rapamycin in patients with hormone-refractory prostate cancer. Amato RJ, Jac J, Mohammad T, Saxena S. Clin Genitourin Cancer. 2008 Sep;6(2):97-102

lewvino's picture
lewvino
Posts: 1010
Joined: May 2009

I'm new on my journey with the prostate cancer. Was just treated with robotic surgery in Aug.
So almost to the 4 month marker. I'm sorry to hear about your latest report but can offer you words of encouragement and prayers. Will hope for the best for you on finding a way to slow the PSA rise down. Bill has some good suggestion with the diet and all. I've been taking pomengranite juice, green tea, green barley, vitamin D and flax seed since about July Time frame. Also have eliminated red meat from my diet and am working hard on contolling how much sugar I consume (That's a hard one for me!) Is it doing any good? Of course there is really no way to tell but there does seem to be some scientific research in studies so I'm giving it a try.

Larry in Tn.

William Parkinson
Posts: 60
Joined: Oct 2009

AUA 2009 - Prostate Cancer: Basic Research - A No Carbohydrate Diet Significantly Prolongs Survival in a Prostate Cancer Xenograft Model Via IGF-1 and Global Gene Expression Changes - Session Highlights
CHICAGO, IL, USA (UroToday.com) - Dr. Stephen Freedland’s group evaluated insulin-like growth factor-1 (IGF-1), which along with insulin is elevated by dietary carbohydrate intake. Both are potent prostate cancer mitogens. They evaluated whether dietary carbohydrate restriction, without energy restriction relative to comparison diets, would slow tumor growth and reduce insulin, IGF-1, and other molecular mediators of prostate cancer in a xenograft model. Male SCID mice were randomly assigned to either a very high-fat no-carbohydrate ketogenic diet, a low-fat diet, or a Western diet and fed to maintain similar average body weights among groups. Mice were injected with LNCaP cells and sacrificed when tumors were 1000mm3.
Having been on the diets before injection with LNCaP cells, they reported median NCKD body weight as 2.4g (10%) and 2.1g (8%) greater than the LFD and WD groups, respectively. Diet was significantly associated with overall survival. Relative to WD, survival was significantly prolonged for and NCKD. Serum insulin, IGF-1, IGF-1:IGFBP-1 ratio, and IGF-1:IGFBP-3 ratio were significantly reduced in the NCKD group. The phospho-AKT:total-AKT ratio and pathways associated with anti-apoptosis, inflammation, insulin resistance, and obesity were also significantly reduced in NCKD tumors. Despite heavier body weights, a carbohydrate restricted diet significantly prolonged survival.
Presented by Stephen J. Freedland, MD, et al. at the Annual Meeting of the American Urological Association

Cheers
Bill

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