My PSA was 227, but lowered to undetectable with Lupron and chemo. Slowly rising now, even though I’m still on ADT. My MD Anderson oncologist is adding Zytiga when it reaches 2.0 again. It’s 1.8 now. And I’m about to have another bone scan while it’s at 1.8. So seems like waiting til 15 is a long time. And, as Yost suggests, want to make sure you are being monitored via bone scans / CT scans to watch for spreading.
Do you have an oncologist who specializes in PCa? That’s very important. If not, let folks on this forum know where you live and I’m sure they can recommmend one.
Since PSA in ‘normal range’ is 0-4, seems like waiting to 15 is a long wait (and seems risky).
What is your overall history with PCa? Did you have a prostate biopsy and get a Gleason score? If so, what’s your score? Have you had any radiation or surgery? Genetic testing?
And someone later in this thread recommended you getting a second opinion or care from a teaching hospital. That seems like sound advice to me. I really like going to MD Anderson for oversight of my case. They and other major hospitals literally ‘wrote the book’ ... and ensure we follow the latest treatment options (like Stampede, Latitude, etc...)
May I ask who your oncologist is at md anderson. Does he/she "specialize' in pc? I am going there for a second opinion. I have heard, the right hand doesn't know what the left hand is doing there, because they are so busy.
The most common place for the hormone sensitive type of prostate cancer to metastasize is the bones, usually starting with the pelvis and lower spine. The only way to know for sure if the PCa is going to the bone is to do imaging. Generally speaking, a CT and T99 bone scan will show you where the mets are unless they are very small.
Another indication you can look at is your ALP (alkaline phosphatase). It's a blood test that can indicate if there is bone activity going on. If you've had that previously measured, you can see if its rising or just check where the level is compared to the normal range.
You said your testosterone is going down, what's the actual level? The absolute testosterone level is more significant than the relative direction its going in. The more of it there is, the easier it is for prostate cancer to reproduce. Up or down doesn't matter to the cancer.
By definition, testosterone levels of less than 20 are considered as "castrate" levels. If your prostate cancer is growing at these levels, you could be castrate resistant. If so, there are second line ADT treatments such as Xtandi or Zytiga available. Docetaxel chemotherapy is also available, but it's more toxic and has worse side effects. Some of us have done it at diagnosis when taking it has a better survival benefit. It does work in most cases even when done after castrate resistance. You should also consider genetic testing to see if you have mutations that allow for targeted treatments.
Good luck with your treatments and keep us posted.
I had read somewhere that it may spread around psa 10, I
Would be nervous to wait till 15 to restart, especially wth that kind of doubling time. I would also suggest a medical oncologist that specializes in Prostate Cancer, In particular one in Acedemia that can be found at major teaching hospitals. I wish you the best.
The first time my PSA became detectable, I had bone mets by the time it reached 0.6. Those were radiated and the PSA was zero for about 16 months. It recurred recently, and I again have bone mets with a PSA of only 0.9
As you can imagine, I would never let my PSA rise to even 4 because by then I probably would have widespread mets.
A year ago I became Castrate resistant when my PSA jumped to 10.0 and testosterone was near zero. Bone scans revealed several bone metastasis but I had no physical symptoms and still haven’t. Zytiga was added to my treatments and today my PSA has been steady at around 0.03.
If you had no metastases, why did you not get definitive treatment (surgery or radiation)? Or are you "waiting"? Gleason 3+3. The fast rise seems like a problem, and not to be ignored.
• in reply to
If you originally had mets in the bone, there almost certainly are mets in the bone now, or at least there is no reason to assume that you do not have prostate cancer cells in your bones. In the context of a rising PSA, there is likewise no reason to assume that only the prostate cells in the prostate are biologically active and the prostate cells in the bone are quiet.
My psa was 5.3 and a digital exam showed hardening with the biopsy a Gleason score of 9. This was 8 months after a TURP which showed psa at 1.8 and no PCa. So 15 for psa seems high to me. I have had radiation, docetaxel (completed late Feb 2017) and am on 6 monthly Eligard for the rest of my life. My psa and testosterone are negligible. In spite of a few side effects ( bowel especially and some nerve damage in legs) I am surviving well. Exercise is crucial ( with rehab in pool and gym I am fitter at 69 than I have been for years). Get treatment asap.
Forgot to say my PCa had spread to both hips, left rib and T10 & T11 vertebrae. Latest bone scan could not see cancer in left hip & rib and other mets are much smaller. There is hope!!
As you know, I have been cared for by the retiring Dr Myers. I have been referred to Dr Drake at Columbia. Snuffy says that “he is a younger and smarter version of me”. You might want to check him out.
Everyone is different. At Psa of 2.3, and monthly doubling, an axumin scan found single 9mm tumor in femur, my first bone met . I went back on ADT3, started xgeva and had sbrt to the tumor. I’m not sure that waiting for psa to hit 15 before starting treatment is appropriate when the new scans are effective at 2.0 or lower. Why 15? Can’t bad stuff happen between 2 and 15?
Bob
Interesting idea!
That rising psa may be due to the growth of capillaries. For psa to be in the blood, one needs cells that are making psa (faster than it is being cleared), and a blood vessel within range for the psa to go into. angiogenesis.
Do you know how much psa rises after a needle biopsy? That procedure briefly creates 12 new paths out of the prostate.
I was under the impression that angiogenesis was the process by which new blood vessels were formed to allow tumors to grow. And that without angiogenisis tumors could not grow more than a few mm. I wonder where we are with angiogenesis inhibitors in Prostate Cancer? I know years ago Myers use to use thalidomide in some men which is a angiogenisis inhibitor, I think Revlimid is also. If we could find a way to stop angiogenisis we could control our metastatic disease.
Thanks Nalakrats, I have heard you talk of gelactin 3 before ,but did not realize the significance, I will order some Pectasol c if I can find some. What form do you get it in? I ordered eco urge ice powder 454 g . Copy from Memorial Sloan Kettering supplement page “Modified Citrus Pectin (MCP) acts as a ligand for galectin-3, which plays a major role in tumor formation and progression (7) (8). Binding of MCP to galectin-3 was shown to inhibit tumor growth, angiogenesis, and metastasis in vivo. MCP is thought to render galectin-3 incapable of binding its receptors that would result in angiogenesis (9). Galectin-3 is also found on prostate cancer cells and in prostate tissue. In another study, MCP was shown to increase the doubling time of prostate-specific antigen (PSA) presumably by binding galectin-3 (6). Pectin was also shown to induce apoptosis in adenocarcinoma cells in vitro via caspase-3 activity resulting in DNA degradation (1). Pectin-supplemented diet was shown to exert antiproliferative effects in mouse distal colon during colonic hyperplasia (2). It also lowered cholesterol in patients with hypercholesterolemia.”
I did not see that Rich, however I do not have diabetes and kidneys are fine, I did see this under mechanisms of Action on Sloan Kettering page:: “ Modified Citrus Pectin (MCP) acts as a ligand for galectin-3, which plays a major role in tumor formation and progression (7) (8). Binding of MCP to galectin-3 was shown to inhibit tumor growth, angiogenesis, and metastasis in vivo. MCP is thought to render galectin-3 incapable of binding its receptors that would result in angiogenesis (9). Galectin-3 is also found on prostate cancer cells and in prostate tissue. In another study, MCP was shown to increase the doubling time of prostate-specific antigen (PSA) presumably by binding galectin-3 (6). Pectin was also shown to induce apoptosis in adenocarcinoma cells in vitro via caspase-3 activity resulting in DNA degradation (1). Pectin-supplemented diet was shown to exert antiproliferative effects in mouse distal colon during colonic hyperplasia (2). It also lowered cholesterol in patients with hypercholesterolemia.” This is from a mouse study, but I am willing to gamble on it at this time
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