I was diagnosed with G9 PCa back in ‘16. After an RP with positive margins and an undetectable PSA I chose to undergo adjuvant RT and a year of ADT. My PSA remained undetectable for 27 months post surgery until early September week when it registered 0.4. Two weeks later I retested and it increased to 0.5.
I traveled to Johns Hopkins last week to meet with Dr. Mario Eisenberger to discuss my options. I expected to hear ADT and possibly chemo as well but instead it was recommended that I do nothing for 3 to 6 months in order to get an accurate gauge on my PSA doubling time. Dr. E stated that there was no proven benefit of starting ADT early, in fact he mentioned that they rarely start it before a patient's PSA hits 10. This run counter to my proactive nature and urge to do "something" now, but I guess I need to follow their advice. I will be meeting with my local MO to discuss further this week. Do anyone have reservation about the wait and see approach under my circumstances?
Written by
shueswim
To view profiles and participate in discussions please or .
This is a controversial subject. The TOAD trial suggested a benefit to early ADT, but with only 5 years of f/u so far, it is still too early to be sure.
I think most MOs would advocate ADT if your PSADT is less than 9 months. You can also get a Axumin PET scan - if distant mets are detected, that is a good indicator that ADT is appropriate.
I was a G8 and had DaVinci in 2016. After RP first PSA was .024 then waited next in October .042 Mid Oct '16 38 sessions radiation. Came out after .080
Since then doubling every 3.2 to 4.5. months. Overall average 4.2 months. This month PSA is 1.7 Without "anything " my Oncologist has yet to pull the trigger on ADT/chemo.
3 scans have shown nothing. Last Friday I had the GA68-PSMA at UCSF. Waiting this week for results.
He too discussed 10. The change for me is now what will Friday show? His thoughts were if that warrants action then of course we start. Now that I'm in"single digits" and if I have a doubling in 3 months then that too is a big consideration.
Feel confident with him. He is close to the researchers at UCSF. His college roommate is there and is part of the team involved with much of the prostate dealings. He consults with them regularly. Feel confident with him (or of course I wouldn't be his patient!)
There are clinical trials for these studies. You could check clinicaltrials.gov .
I f you do not qualfy, perhaps you could get it done at UCLA (cost around $ 2700, Dr.Wolfgang Fendler
310-825-3617) . If metastases are detected with this study your situation will have to be re-evaluated .
There is a clinical trial for the vaccine Prostvac for patients with BCR when they reach a PSA of 0.8 or higher. This vaccine does not work in castration resistant cancer but it seems to work in hormone sensitive cancer. I had this vaccine in 2007 and stopped the progression of the PSA for 6 years.
I believe Dr. Fendler is part of the faculty at UCLA doing the Ga 68 PSMA studies. I do not know what their requirement are at the present time. You may need to call them and see what they have to say.
Another UCLA doc involved in the PSMA trial is Johannes Czernin in Nuclear Medicine. Requirements to get it free include having radiation already scheduled and for the R.O. to agree to use results in the treatment planning.
I don't know the answer to your question but here are some hopefully relevant thoughts.
First, it's hard not to take Hopkins oncologists seriously. They are among the world's leading prostate cancer experts in both treatment and research.
Second, there are differences in the kind of treatment that will help depending on the aggressiveness of the cancer. For example, it is my understanding that the combination of ADT + chemotherapy is only better than ADT alone in patients whose cancer is quite aggressive. If it's not very aggressive, then ADT alone does just as well and the side effects and risks of chemo are all for nothing. I believe that Tall_Allen has posted on this issue in the past and has a blog post that discusses it. If that's right (Tall_Allen and Dr. Eisenberger both know much more about this than I do) then you don't want to rush into chemo unless and until you know it's helpful, and you may have to delay treatment to find out.
As for the best PSA threshold for taking action, as Allen says, there seem to be different points of view. 15 years ago, when I was diagnosed, Dr. Patrick Walsh, possibly the leading PCa urologist in the U.S. was saying there was no benefit to ADT until a patient is on the verge of experiencing symptoms. We now know that that is wrong, but I don't know whether treating 0.5 extends life longer than waiting until 10.0.
PSA 10 is not a target. I believe all PSA numbers above 4 are suspicious and require treatment. The only caution is hormal resistance and hoping if you wait this wont occur when being treated. They call it CRPC (Castrate Resistant Prostate Cancer.)
The term medical castration which to me is a horribly wrong expression. Firstly it is not castration as it is not permanent. It reduces Testosterone to castrate range. To me thats not the same as surgical castration which is abhorrent to men.
If there is no reason to have a PSA at all any number means trouble. If you get any meaningful info out of the exact number Id like to know exactly how the treatment might be altered to benefit the patients outcome? To me its like being a litlle bit pregnant...
You either are or not and waiting for a number seems senseless to me.
If by "palliative" you mean that the treatment only reduces symptoms but does not extend life, I think we now have evidence that ADT is more than just palliative. The advanced ADT especially (abiraterone, enzalutamide, maybe apalutamide) have been shown to extend life and even the traditional LHRH agonist form of ADT does actually kill off significant numbers of tumor cells and does hold down the rate of tumor cell replication and therefore reduces the number of tumor cells that might be mutating into more aggressive forms. This too does extend life for many men.
I was referring only to castration therapy. When shueswim referred to ADT there was no reference to abi, enz or other add-ons.
Apologies for the confusion.
But I read all the time of "abiraterone was also approved for use in the new population of asymptomatic or mildly symptomatic patients having failed ADT" [1] & "novel therapeutic agents in conjunction with ADT" [2], etc.
I have no problem with Enzalutamide being classed as ADT, although I never saw Casodex referred to as such.
First let me say I miss you on our site. You are one of the most knowledgeable people I know.
With Lupron maybe we have to redefine cure. If one demises with PCa and not from PCa to me that is a cure for PCa. We have an old age endpoint where many causes can do you in. So its a race to the finish line. If we can abate one of these killers then we are good stewards of our bodies and lives.
No one knows Lloyd Ney and his group of Lupron advocates whose lives were extended many years when all were considered terminal,forsaken,hopeless and in terrible agony. Mr Ney petitioned Congress to bring Lupron into this country.
Was that for nothing? A friend 81 hard as a rock prostate, large tumor PSA in excess of 300 did Lupron and died age 96 not from PCa. He was terminal for 15 years...no pain, worked every day and was physically active and lived alone..sharp as a tack.
Hi Patrick, as a recent reader of ADT topics, wondering about reasons for first-line Lupron etc. therapy option restrictions vs. some of the newer ones - considering studies going back about 20 years indicating they may initiate EMT and neuroendocrine differentiation.
When I was diagnosed, there was no CRPC. ADT failure was termed 'refractory'. The androgen receptor [AR] was thought to become irrelevant.
The commom PCa cell lines, that appear in almost all of the cell studies are LNCaP (lymph node), PC3 (bone) & DU145 (brain).
PC3: "These cells do not respond to androgens" "and do not express PSA" [1]
"DU145 are not hormone-sensitive and do not express prostate-specific antigen" [2]
But suddenly (after decades) it was discovered that the AR continues to have a role after ADT failure in actual cases. & so began a major effort to shut down the sources of all hormones that might convert to androgen.
Frankly, I was dismayed. The prospect of life without any steroid hormones wasn't very attractive to me.
The continued focus on the AR axis has meant less research money elsewhere.
The lesson from basic ADT (Lupron), Lupron+Zytiga & Lupron+Xtandi, is that failure is almost inevitable, & that the more we try inhibit AR activity, the greater the odds that we will not be able to manage the cancer that emerges. My doctor tells me that his patients' cancer really takes off after Zytiga failure. We just aren't prepared for the types of cells that emerge.
For someone who must be on ADT & wants to maximize its effectiveness, I suggest that a statin is essential - to limit cholesterol uptake (the starting point for all steroid hormones), & to stop PCa cells from making their own cholesterol. In addition, since the whole point of ADT is to stop AR activation by DHT, Avodart should be used. In other words, not only shut the barn door, but shutter all the windows too.
Today, 1st of the month, I inject testosterone. I'm pretty much following the BAT protocol. Rapid alternation of high T to castrate T within each month may interfere with the adaptations that plague current therapies.
Great post and thank you for this information. What dose of statin is thought to be effective. I am on 10 mg atorvastatin (past 5 years) and was thinking of increasing that dosage (which my GP is willing). So I am deciding between 20, 30 or 40 mgs?
My husband has a similar history and the uro-oncologist is suggesting stopping ADT and doing a Ga 68 PSMA scan when PSA is high enough. Depending on what is found, the plan is to do SBRT. HIs argument is that it's better to do this now while he's hormone sensitive and cancer is not as aggressive. Did your doc mention treatment for oligomets after Ga 68 scan?
I have heard of EBRT, IMRT and now cyberknife. All of these focus on the tumor.
When they say focus.......what they mean is intense radiation controlled by a computer...yes its precisely targeted not to harm normal tissue.Only intense radiation kills cancer cells. We are led to believe only a small portion of the prostate is affected..I dont believe it is true. More than likely you will not have a functional prostate. But we may be talking about salvation RT which doesnt have the same result because the prostate was surgically removed.
He mentioned it briefly, but the availability of Ga 68 PSMA scans appears to be a problem. I located a list of current clinical trials utilizing these scans, and will be discussing with my local MO later this week.
I read your history with serious interest. I did ADT in 2004 and had no surgery or RT.
For a period of 13 months my PSA was .005.There was a debate as to when I should start the Leibowitz protocol after doing the standard protocol. Should I wait and then do the protocol or just start the protocol now. While my story doesnt match yours the feeling is similar. Everything went ok and as a result I had 18 months of ADT of some form.
At some point before I took Prostasol and cut my PSA in half in 3 months but my GS went to 9 from 7. I went to MSKCC for a second biopsy. You cannot do a biopsy with Prostasol in your system. So my GS went from 3+4 to 4+5 and a pathologist from Hopkins called me to find out if I was on Lupron. The Prostasol may have had DES in it and somehow that affected the look of my cells. After ADT 14 years later my PSA is 2. But I wasnt really a 4+5.
What will you gain when you learn your doubling time? Will that alter your treatment?
If you are hormone sensitive is the question.What if you are not? Why find that out 6 months from now? If you do ADT at all do the Leibowitz protocol and stay away from chemo.
I am also at Hopkins and received the same advice. I believe my RO and Mo when they tell me that if my PSADT stays high there is no need to hit it hard early. This will hopefully allow me another couple of years off of ADT with no difference in survival time.
I would suggest looking into getting the PSMA Pet Scan at Hopkins or NIH (clinical trial) and try and find out where the cancer is hiding. I just had the scan and it is limited to one lympth node of which i will talk with my docs about how to treat.
We are with a top 5 PCa hospital and in good hands. I use the information on this this invaluable for to ask questions and discuss alternatives.
My MDA MO is recommending Erleada after a rapid DT (less than 3 months) of my PSA to 1.5. This is after a very quick break through of ADT. Auximun scan shows no mets and localization of the cancer in the prostate bed. Does anyone have experience with Erleada vs. Provenge? My concern is in line with what Patrick expressed when the cancer emerges from drugs like Zytiga, Erleada and how to treat it then.
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
PSA rising - When to get a PSMA PET scan?
ADT vacation for 10 months
mcp1941
PSA Expectations after SRT with Concurrent ADT
