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Cancer: Prostate Message Board

Cancer: Prostate Board Index

Hi Rod,

Welcome to the Board!

Your background so closely resembles mine that I almost feel like I am thinking your questions through for myself. :) It’s an interesting coincidence that this is my 2,000th post. (I was diagnosed with a well elevated PSA – 113.6 but would have likely been close to 27 a half year earlier, Gleason 7 (4+3), extension outside the prostate per DRE, four rounds of intermittent ADT3 initially with Lupron, Casodex, and finasteride, being around long enough that the medical oncologist who was my key strategist retired, and PSA being monitored with an ultrasensitive test. While I was diagnosed about ten years before you and at the younger age of 56, I did not have radiation until 2013, after you did.) I too get extra focused when it’s time for my quarterly PSA tests, which may be the same as yours, but are based on a less sensitive ultrasensitive test that has a lower limit of <0.05. However, while our cases have some similarities, each of us is different, and so may be the best course for us at this point. That said, I know this territory pretty well.

Would you mind confirming your PSA trend? From your post, your PSA was 0.001 but then increased to 0.06 one year ago before declining six months ago to 0.015, and then increasing to 0.036 at present. Did you mean 0.006 instead of 0.06?

In any case, your present PSA and mine may be very close. My doctor formerly used a PSA sensitive to <0.01, and I got to that lower limit during my first two rounds of IADT3, but he had to send it out of state for processing, and that added about a week. (Back in 2000 I was the first patient to request an ultrasensitive PSA, and of course the first to get it at that large practice of many oncologists.) After radiation in 2013, and then after my course of supportive ADT ended, my PSA rose to 0.02. At that point my doctor switched to a local test with a lower limit of <0.05, which is, of course, higher than your recent PSA of 0.036. My PSA has never been higher than that lower limit since my radiation in 2013.

However, my testosterone level has settled in the 90 to 110 ng/dl range, rather low, but good enough in my mid-70s. Is your testosterone of 1.2 also in ng/dl units, or does France use other units? As we both probably know, this could be significant.

My understanding from your post is that you ended ADT3 about seven years ago (9 years at diagnosis, – 2 years of ADT); is that right? If so, then your PSA would have been quite stable for a number of years but rose to 0.06 a year ago, before a drop, and then two increases but still a very low level of 0.036 currently, in the context of having an intact but radiated prostate.

You appear to be calculating doubling time using the values 0.015 and 0.036. One possibility for the increase is that your prostate is experiencing a late recovery from the radiation, or from ADT3, or both. I have no basis for suggesting a late recovery other than that many of us see a similar trend but years earlier after treatment, in other words, closer to treatment. In my own case, after starting my vacation from ADT (supported by continued finasteride) following my first round of ADT3, my PSA rose from 0.01 on 9/19/02 to 0.13 on 11/6/02, a doubling time of .4 months – extremely rapid! The next test on 12/5/02 resulted in a PSA of .2, so the doubling time based on that and the November result was 1.5 months – still very rapid, but noticeably slower. What was happening was that healthy cells in my prostate were recovering, and the growth was rapid, but mostly not from cancer. I have used the periods during my vacations from ADT3 from my PSA reaching about 5.0 to reaching about 10.0 to gauge a truer doubling time – free of the rapid increase from initial healthy regrowth. Those doubling times, before I was apparently cured in 2013, were each in the three to four months range, much longer than the early rapid increases.

My point here is that the early doubling may not represent what the situation really is. By the way, for my first two rounds of ADT3 and vacation, the trigger my oncologist and I used to restart ADT3 was 10, partly using that relaxed trigger because my baseline PSA had been so high. (We actually used a trigger of about 20 for my third round, but that’s a different story.)

Also, if that 0.06 is the right number and not 0.006, there might be some variation caused by lab processing or choice of different ultrasensitive PSA kits, or even one of those rare lab errors, rather than a true steady upward trend over the past four readings.

I feel you have a basis for concern but not for worry, at this point; be watchful and alert, but confident and not afraid.

I have thought what I would do if my PSA started rising above <0.05. I first plan to have a retest in a month instead of my usual 3 months. Then, if the increase is confirmed, I plan to add one element to my anti-recurrence shield: the old diabetes drug metformin. Recent research over the past few years and understanding of its mechanism of action is suggesting that it packs a good anti-prostate cancer wallop. I’m already on good lifestyle tactics, including a Mediterranean diet, rest and an anti-stress lifestyle, and exercise.

I also take a statin, as that helps me with cholesterol and is associated with increased success against prostate cancer. I am also on the drug dutasteride (Avodart®), to which I switched after many years on finasteride as I was trying to increase my time off Lupron and Casodex. It did seem to help, and it’s something you might want to try as dutasteride is known to be somewhat more potent against DHT (dihydrotestosterone) than finasteride, and, of course, DHT is a far more potent fuel for the cancer than testosterone. Some of us still produce substantial DHT even when testosterone production is severely curtailed.

Research suggests strongly that it would not be time for you to start Taxotere® should you restart ADT. I saw a recent paper reviewing findings for men in the key trials (CHAARTED, STAMPEDE, AND GETUG, which I believe was French or Spanish) that compared results for men with a high level of prostate cancer metastases to men with a low level of metastases (all were metastatic). The finding was that early chemo definitely and substantially helped men in the high metastasis group, but it did not help the men in the low metastasis group. I noticed that in the CHAARTED results at least a year ago; it’s a pretty clear pattern. You are not even metastatic, so chemo looks like it would be premature.

Xtandi® (enzalutamide) might be a good choice if it is available. It is now only approved in the US for men who are resistant to ADT and metastatic. Based on good results from a trial, we expect that it will soon also be available to men who are not metastatic but still resistant to ADT. The new drug Erleada® (apalutamide, approved in the US just weeks ago) already is so available. However, you would almost certainly still respond to ADT, so, at least in the US, you would not be eligible for approved prescription of Xtandi® or Erleada®. However, you might be able to get it, were you in the US, using “off-label” prescription; that could negate insurance coverage. I’m curious what the situation would be in France for prescribing these two drugs.

Because you are over 80 years old, I like the idea of using an antiandrogen like Xtandi® as the basis for treatment rather than an LHRH-agonist (like Zoladex®) or an LHRH-antagonist (Firmagon®). Similarly, if cost and access are issues, bicalutamide (Casodex®) plus finasteride or dutasteride would also probably work quite well.

If you do have prostate cancer that is on a recurrence path that is serious and not mild, you should still be able to slow up the cancer and gain time for technology to keep improving, which it is doing at a rapid pace. For instance, imaging and precise treatment of “oligometastatic” recurrence could be curative, or at least knock the cancer way back again.

Good luck with this! :cool:
Hi again Rod,

Here are some thoughts.

[B][U]Rapid growth/low T[/U][/B]: Yes, what appears to be rapid growth, if sustained, would make me worry too if I had such a low testosterone level. There is still a chance, in my layman’s view, that you are experiencing a late but normal recovery from radiation and ADT. I would want PSAs every month, or at least every three months for a while to see if the PSADT slowed, stopped, or reversed versus increasing in that exponential pattern characteristic of prostate cancer.

[U][B]DHT, dutasteride, finasteride[/B][/U]: Have you had your DHT level checked? I imagine it is pretty low because of the finasteride and extremely low T, but I would want it checked. The doctors I have followed who have used a lot of ADT, including ADT3 and IADT3, now favor dutasteride rather strongly, but apparently about 10% of us have genetics that don’t allow us to take advantage of dutasteride while we can use finasteride.

[B][U]Dose of metformin and trigger[/U][/B]: In the US the pills are each 500 mg, and four of them makes a full daily dose for diabetics. However, while most of us tolerate metformin very well (many with no side effects at all), some of us experience some nasty side effects at the higher doses (and probably that’s true for a very few of us at the lowest dose), with the side effects disappearing when the drug is stopped. The US FDA website and published studies detail those side effects and doses, but there is a practical solution, as advocated by that now retired oncologist who has used the tactic effectively in his practice: start with the lowest dose – one 500 mg pill in the morning, and if it is well-tolerated after two weeks add an additional 500 mg pill in the evening; do that two week routine again, morning and evening, until the full dose is reached without intolerable side effects. If any of the increased doses are unpleasant, drop back to the lower dose that is well tolerated. As for the trigger, I feel you could wait to see if there were encouraging changes to your PSA over the next few months, or you could start now. I’m not aware of a downside to metformin other than side effect tolerability. Metformin is an old drug with a very long track record and therefor has been thoroughly studied and reported.

[B][U]Xtandi® and trigger[/U][/B]: If cost and access are no problem, you might benefit from early use if that pattern of PSA increase looks like a problem. Two concerns strike me at the moment. First, Xtandi® will very likely knock your PSA down again if recurrent cancer is the cause. While that’s what we want, it will preclude imaging of very small metastases if there are any, as it seems the best scans need a PSA of at least 2 to do reliable work, though they sometimes are able to spot metastases at lower PSA levels. If you have just a few metastases, current research suggests a reasonable chance of success with spot radiation or spot surgery to eliminate them. Emerging technology may make scans even better and able to get results even when the PSA is lower, but you may have to make a decision on Xtandi® or Erleada® in the near future.

[B][U]The second concern with Xtandi® and Erleada®, also with Zytiga®[/U][/B], is that the profound androgen deprivation they achieve seems to foster changes in some of the cancer cells to the “small cell”/neuroendocrine type that can be very dangerous and aggressive. I learned that in a DVD of a conference of experts who presented to patients, and they seemed well aware of this phenomenon and concerned about it; however, it is hard to find in published research or abstracts, which is odd. That retired doctor has not seen much of that transformation in his clinic in contrast to what his colleagues are seeing, and he believes it is because he is using estrogen skin patches to protect against bone mineral density (BMD) loss due to loss of testosterone while on ADT. (By the way, have you had your BMD assessed with that very low T? Do you use tactics to protect BMD?) Also, men with metastatic prostate cancer who had the gene mutation AR-V7 did not respond to Xtandi® and Zytiga®; I believe there is now a commercial test for AR-V7. There is some evidence that metformin fosters the effectiveness of Xtandi® and Zytiga®, partly by affecting AR-V7.

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