PC TO THE BONE

Is there an indication when prostate cancer is heading for the bone? Is it when there is a PSA rise (doubling, tripling), PSA number etc?

My oncologist says to restart ADT when the PSA is 15 regardless of the doubling time.

Usually my PSA doubles every 3 months but the last 3 months it is tripled.

My concern is that starting ADT (Lupron & Cassodex) at 15 with very rapid PSA rise might mean it is heading for the bone.

Just a note that my Testosterone is actually decreasing whilst the PSA is rising (does this mean anything??).

Thank you so much for your opinions.

35 Replies

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  • Has your doctor ordered a new bone scan?

  • Yes I did a bone scan which showed a suspicious spot on my spine but the oncologist said it wasn't a met.

  • You may want to say to your oncologist that 15 scares you, and you'd rather start at 5.

  • This is what I will do.

    Thank you so much.

  • I am going to ask for an MRI and a bone scan.

  • 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.

    Best of luck! We are pulling for you!

  • Thank you so much James for sharing your experience. Yes I do have an oncologist who says when my PSA gets to 15, then to start ADT.

    BUT I have been told with a rapidly rising PSA (doubling every 3 months) that it could go to the bone and I should do ADT when my PSA get to 5.

    It is right now at 3.5

    Best regards,

    Marguerite

  • 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...)

    Best of luck!

    James

  • Who do you see at MD if may ask. I got a second opinion from dr rujoe (spell?)

  • 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.

  • Hi Gregg,

    Thank you so much for your reply.

    I didn't know about the ALP but will get that test done.

    My testosterone is 13 right now. Down from 20 a year ago. But my PSA is doubling and just in the past 6 weeks it tripled. The PSA is 3.5 right now.

    Thank you so much.

  • 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.

    Dan

  • Thank you Dan.

    I have read the same which is about 10 PSA may go to the bone.

    Which is why I am nervous about waiting to 15, particularly as you said with my doubling time.

    Many thanks and best of health to you.

  • 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.

  • 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.

  • I was dx with very advanced stage 4 with mets all over spine with PSA 11. 5 months before PSA was 3.1. 15 sounds high

  • 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!!

  • Hi Marguerite.

    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.

    Rex

  • 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

  • Bone Mets are not always related to a specific PSA number. When PSA is Doubling, in short month or 2 month cycles, it is an indication, of the beginning of Angiogenesis. Angiogenesis, is a process, where Pca cells, get together thru an agglomerating process making use of a chemical that the Pca cells produce, identified as Galactin-3--there is a dividing and a continuing of sticking together, as they grow. Then at some point they take off, usually heading to bone, thru the lymph or blood system. As this happens PSA increases, as there are more Pca cells.

    But this above is not the purpose of me writing. There are cases of men reaching nadirs of undetectable, after surgery, radiation and ADT, or in combination of these that when some time down the road, a PSA shows up. THERE ARE MEN WHO AT 0.2 COMING FROM ZERO, HAD SHOWN BONE METS. There is no known formula, as we have many many pathologies, that all act according to their own time frame--or mutational process.

    So when you have a doubling, in a short time frame, or in the case of many men with PSA's of under one, after being zero--time is right to get sensitive scans. Prominent Oncologists will scan you, when this happens.

    As to T reduction, could it be you have more cancer cells now and that your constant T level is being used up by the new Pca cells, as they take the T to their Androgen Receptors, using up available T. Not anything but a big guess.

    Nalakrats

  • 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.

  • Almost exactly----Pca cells have to get together before forming new highways[Blood Vessels]. When they are unformed they have no strength, as they are not in a gang[Tumor]. Galactin-3 is the identified, [I believe it is a protein], have not read on it for a year or so---that allows Pca cells to stick together. Then the Pca cells get going, as they are now strength in numbers. I am being simplistic here. But you should get the drift.

    But as to anti Angiogenesis materials[drugs or Supplements], I am aware of the use of thalidomide---but there was no measurable research at that time. If it halted angiogenesis, we knew not why.

    Today we have measurable data as to Galactin-3. The theory is, if you eliminate Pca cells from creating Galactin-3 there is no angiogenesis. So the theory is!

    One material in Phase 3 Clinical Trial, that does prevent the formation of Galactin-3---check at NIH---is Pectasol-C. Also In Israel a Phase 2 has been completed. I read the Israeli data, that they prove statistically significant, the inhibition of Galactin-3 with Pectasol-C. Also they are showing some Pca cell death. And of course without cell growth, and some cell death, you have reduced PSA's.

    This Pectasol-C, is being used by some men here--I am one--been on it since the Israelis started their Phase 1 Trial in the beginning of 2016. So I have been using for about 20 months.

    Nalakrats

  • 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.”

    Dan

  • Amazon and Vitacost is where I buy.

    Nalakrats

  • Do you remember reading that Pectasol-C was not good to take if someone had kidney disease or diabetes?

    Rich

  • 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

  • Thank you for the information.

    Rich

  • No I did not read anything to that. I take Metformin in case of ADT inducement of pre-diabetes, and all my mineral supplements are Amino Acid Chelate---which makes elimination thru the kidney's easy. I guess you saw Dan59 and his comments on MCP. Reads like from the study, I read.

    Nalakrats

  • Thank you for the reply.

    Rich

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