Advanced Prostate Cancer
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Choline PET scan

Is anyone familiar with Dr. Eugene Kwon from the mayo clinic and his work in Oligometastatic prostate cancer

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I had Kwon's treatment....PSA was 1 and he told me to wait until it was 2..had all the treatments and $450,000 later the P$A was going up...total waste of money

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Thank you

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Did insurance cover anything?

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Yes it looks like the p yes it looks like The PS MA pet scans look to be about 10% more accurate.

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There is really very little evidence to back up Kwon's beliefs. So far, there has only been one pilot trial, and the results were equivocal and disappointing.

pcnrv.blogspot.com/2017/12/...

And if you decide to do it, you can do better than the choline PET scan.

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TA

Thanks for your incisive analyses including Dr Strom’s observation. Both times I used MDT (to pelvic lymph nodes and later to femur) I also used ADT 3. I agree it makes no sense to use MDT to delay ADT but as an adjunct. I believe I’ve read that some men with low volume Gleason 8-10 have had durable remissions as a result of treating oligomets as they pop up. Am I misinformed?

Bob

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Yes, you are misinformed. As I said, there has only been that one small clinical trial that compared MDT to observation.

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Has there ever been an attempt to coorelate Tumor volume at pathology with prostate specific or overall survival?

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Yes it looks like the PS MA scans are 10% more accurate. I don’t know if it makes a difference or not. My PSA is 92.

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I don't think it will make a difference at a PSA of 92. At low PSA, PSMA scans have a detection rate about 5-fold higher than choline scans.

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"There is really very little evidence to back up Kwon's beliefs."

Just to clarify, this refers to his decision to treat individual metastatsises, as opposed to using chemo or other systememic treatment.

Is that correct?

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Correct. There is good evidence that systemic therapy delays progression.

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What belief does he have that you feel is incorrect? He does imaging, no? You dont like the C11 choline?

Oh! You are saying that in some cases, where the scan shows one hot lymph node, or one hot met, and he treats it, and gets long term clear scans, that this is a mistaken treatment? I doubt that the patient in these cases agrees with you.

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His belief is that metastasis-directed therapy provides long term remission or cure. That belief is unfounded by any data currently available.

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He does have a few patients in long term remission. How many I don't know, but the fact that there has not been a controlled trail, does not mean that these people do not think the world of him. I saw him once, and I was blown away. He had no tricks for me unfortunately. I've been to Weil Cornell, to MSK, to Johns Hopkins. He is way more cynical than any of them. I think that's the word.

He agreed that the NCCN guidlines needs to add a module on planned giving and casket selection.

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I've met him too and was impressed by him personally. But that doesn't make his hypothesis correct, unfortunately. Many MOs have patients in long term remission.

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Long term remission? Is there a study of those patients? To see if there is something to be learned? Here is one study -

ncbi.nlm.nih.gov/pubmed/288...

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I agree that there may be benefit to treating the prostate and the entire pelvic LN area when any cancerous pelvic LNs have been detected (N1). I wrote about that and other similar studies in this article, which you may find interesting:

pcnrv.blogspot.com/2016/08/...

However, that as nothing to do with metastasis-directed therapy that Kwon believes in.

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Thanks

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What is it that you think he believes in?

My impression is that if he sees one or two hot spots that seem to be the sources of a PSA of say 2 or 3 after treatment to the primary, he is willing to advocate for radiation and/or surgery, which the radiology department or surgical department needs to buy into.

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He believes that metastasis-directed therapy can lead to lasting remission or even cure- a belief that has no evidence to back it up. Silly dog-and-pony shows shown to desperate patients are no substitute for real medical evidence.

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I had the Kwon/Karnes choline and plnd in 2013. PSA 17 gs 8 post rp and srt. Goal was to delay adt not cure. Plnd reduced PSA to 2.3. But it missed a few nodes shown by the scan. PSA was 49 a year and a half later. Conclusion: slower doubling time will yield longer delay of adt (duh) and I achieved limited success. I call it a qualified failure. Don’t expect a cure. If you are not averse to adt or adt combos with docetaxel zytiga etc, then systemic therapy should be considered. I work full time now age 61 (Dx age 52) and seek to minimize risk of any cognitive decline as my secondary goal of controlling the pca. As with all pca treatment choices no one best answer and you need to consider your case and goals individually.

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What is plnd?

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Pelvic lymph node dissection

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Thank you

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You can read the Kwon/Karnes study results for the choline scan followed by plnd procedure in the 2014 Uro Today article:

urotoday.com/recent-abstrac...

And this 2018 report from a small English study:

meetinglibrary.asco.org/rec...

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Thank you

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One has to be very careful in interpreting studies like this. They really show nothing. There is no way to know, based on the data they provided, whether the treatment was "useful" or not. We have no way of knowing what the distant progression-free survival would have been had they not received the MDT treatment.

pcnrv.blogspot.com/2017/05/...

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The problem is that treating PSA is not the same as treating the cancer. There is no question that MDT will eliminate larger mets that are putting out the lion's share of PSA (only mets that are large enough to create their own blood supply put out PSA into the serum - smaller mets do not). So if you start by ASSUMING that ADT is delayable if the PSA is low enough, and then you reduce the PSA with MTD, but not all the other metastases, you have may have only tricked yourself into believing that it was a good move to delay ADT. Recent data has shown that early systemic treatment eliminates most of the mets you can't see as well as the ones you can.

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"Recent data has shown that early systemic treatment eliminates most of the mets you can't see as well as the ones you can."

1 That makes a lot of sense.

2 Let's say you remove those large PSA generating metastatsises. Will that impair the ability of a subsequent scan to find the remaining small Mets because of the reduced PSA levels?

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Tall,

What you have said is quite true. There is also the possibilty of neuroendocrine tumor or high gleason PCa which do not typically produce as much PSA. Controlling the PSA is, as you said, only controlling a biomarker, which however in many circumstances (especially recurrent PCa) is a good surrogate for growth of PCa. Scans, CTCs and biopsies are needed to confirm the actual growth of the tumor. Scans themselves can be misinterpreted and lack specificity. Clearly the patient has to decide what his goal is. My goal was and still is to avoid risk of cognitive decline with ADT. When I was diagnosed 10 years ago at age 51 (PSA 136), I could not see myself on ADT for several decades. I also believe there is treatment mediated selection pressure which causes, in part, the AR receptor to mutate and become castration resistant. So surgery and radiation have been my main treatment modalities to date, although I did start IADT with 50 mg of bicalutamide 3.5 years ago. I am still hormone naive. The MDT approach I took in 2013 was not curative and I knew there were other systemic treatments available with better statistical outcomes. Today, there are even better ones with the approval of second line anti androgens and combination therapies with ADT. If my goal were to eradicate the PCa (which is very unlikely in any event), I would have already tried 3ADT plus docetaxel, then plus zytiga and prednisone, then plus enzalutamide, then apalutamide, and then throw in some provenge and radium 223. No thank you!! But for others, it might be the right thing to do. What gives me comfort is that I will never know if I was right or wrong because I have no control group and every study recommendation is based on median results, not the individual case. Best regards!

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How can you say you have not had systemic treatment if you had iADT with 50 mg of bicalutamide for the last 3.5 years? That is exactly the kind of systemic treatment I think is necessary. I believe you have to treat what you can't see as well as what you can see, and you are doing exactly that. BTW- I know a patient who only takes two 50mg bicalutamide pills per WEEK (with raloxifene) and is controlling his PSA quite well.

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I was avoiding systemic treatment in 2013 when I decided to go with the plnd. I tried to avoid it then but as I said, it was a qualified failure becuase it only delayed ADT by a year and a half. With respect to the bicalutamide, I was told the half life of it is about a week, so the example of the patient you know who takes it only twice a week makes sense. I may try that too. I am now 7 weeks on and 6 weeks off, with PSA ranging between 20 and 50.

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Raloxifene. That is a SERM. Is he Erik Castle's (MAYO CLINIC, AZ) patient? Erik talked about that years ago, but has said nothing about that lately that I have seem. I thought it must have been a bust.

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He is taking raloxifene (rather than tamoxifen) to prevent gynecomastia - a prevalent side effect of casodex. He finds that tamoxifen depresses his testosterone levels further.

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Tall_Allen: Erik Castle gave a talk at the 23rd Annual Perspectives in Urology, Point Counterpoint, Med College of Wisconsin. He talked about the role of the estrogen receptor in prostate cancer. Quite interesting. But really he is the only one that I know of that is talking about it. Have you heard more???? (related to your raloxifene comment)

ocpe.mcw.edu/sites/ocpe.mcw...

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are you implying that the PSA goes up when the cancer is contained in the prostate because of angiogenesis?

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Yes of course serum PSA goes up when there are tumors in the prostate because tumors create their own leaky blood supply,

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Dr. Kwon is at the Mayo Clinic in Rochester, MN, and a very well respected PCa researcher. Howevear, the caveat to the choline PET scan is that it is his baby, so his papers and You Tube videos on it, while interesting and compelling, still smack of being infomercials for it. Perhaps with more case studies or clinical trial results the relative advantage of the choline pet scan might be better demonstrated.

If it is superior to other scanning methods you would think the Mayo facilities in Scottsdale and Jacksonville would immediately hop on board, but (so far) they haven’t.

Within the past year, after watching Dr. Kwon’s You Tube videos, I asked my MO at the Jax Mayo if they used it. He said no, but they use the Axumin PET scan You can Google it for more info) that is equally accurate. I may be wrong about this, so don’t hold me to it without further research, but apparently the choline scan requires special equipment, and the radioactive choline contrast agent has such a short half life that it has to be made up just before each patient’s scan is done, which makes it a very expensive option for little if any improvement in quality over other currently used contrasts currently used for similar purposes. Anyone who reads this, please feel free to correct me on that point, because what I said above is just my own humble non-medical opinion based on what I have read and heard. Also, keep in mind that different types of PET scan contrasts are used for different purposes.

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Very good since your response, thank you

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You are quite right. Mayo spent a lot of money to set up a facility to produce C11, including an in-house cyclotron and an organic synthesis machine to generate the C11 Choline on site (not to mention the cost of patents and FDA approval).

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When I talked to Dr. Almeida, he indicated that he thought his c11 acetate scan was comparable to Kwons c11 choline scan.

He also expressed the opinion that in his hands the acetate scan was more accurate than the Auximin scan. He does both, and he did a dual test of both on a trial of 30 patients.

He also mentioned that the acetate scan is showing promise on a number of other cancers. I forget the list he rattled off, but it included: breast, colon and pancreatic.

He did admit that his acetate scans are no longer economically viable because

1 Auximin is now covered by Medicare

2 the equipment costs for acetate

3 acetate is generic. It can't be patented, so it is close to impossible to get money for more clinical trials of acetate.

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A couple years ago as I was coming to terms with my cancer and in full panic and research mode, I went to Mayo a few times to see Dr. Kwon. Suffice it to say after learning more about the latest imaging techniques and treatment protocols, I went to Johns Hopkins for a PSMA PET scan and chose a doctor at Dana Farber Cancer Institute in Boston.

In case you haven't seen this, here is a link to scan information..

pcnrv.blogspot.com/2016/12/...

All the best,

JDM

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was the PSMA at Hopkins part of a trial; didn’t think there were PSMA’s available in US that were not part of trials?

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Yes, I should have been more specific. It was the 18-FL PSMA PET through a clinical trial directed by Dr. Ken Pienta's lab.

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Yes, I am closer to Hopkins and would consider the PSM they scan but it is still in trial. Thank you for sharing!

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I don't know. If you look through the clinical trials database, they have several going. I'm not sure which would be most appropriate in your situation.

clinicaltrials.gov/ct2/resu...

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Thank you, I will look into it. Still going to see Dr. Kwon but of course nothing precludes me from participating in the study as well. I appreciate you!

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i have seen Dr Kwon and I think he is beyond great. Very few doctor hope for a long term regression, but Kwon will go for it, and he gets some. Each one is a life saved.

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That’s what I’m hoping for too! Thx

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Pienta is also cool! He has been interested in the micro-environment of cancer for a long time. I just heard about MDSC (myeloid derived suppressor cells: a fancy name for wierd looking cells in the non-white-blood-cell line (cough: the red family), but strangely wierd. Not "leaf" cells, not fully differentiated cells, but the other kind: "stem", for lack of a better word. Cells that probably should have become macrophages, but hung around with a bad crowd. Anyway, he is looking into shit like that. Juvenile delinquents.

I saw him for his pleurixifor trial. A clever use of a black box warning. Lemons to lemonade. Unfortunately I was too healthy.

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So the "18-FL" PSMA compound is a conjugate drug? More or less for sure, right?

It has a ligand for PSMA, and it has a payload (18-FL) that emits positrons, so you can see where the ligand part sticks onto the PSMA (on the cell membrane) by detecting the positrons in a PET scan. The question is what PSMA ligand are they using; what are they using to stick to the PSMA, the binding site on the prostate cell membrane.

It could be a full PSMA antibody, like j591, which has been around for a while, and seems to be struggling, or they could have chopped off just the heavy(?) chain (one arm of the Y antibody), or they might have come up with an altogether new tiny compound that binds to the PSMA. Like the "617", whatever that is.

Well the JH site says " [18F]DCFPyL, a second-generation fluorine-18-labeled small-molecule PSMA inhibitor", so it looks like it is a "small molecule" ligand, not J591, but not the "617". Whatever...

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These scans are available in Germany and Australia. I am told Australia is the much cheaper of the two, and that it's low cost more than pays for the travel.

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UCSF does ..I had one in Jan,2017 did not find PCA but my PSA still rise back on Lupron. Medicare covered

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Kwon directs my treatment. I have had ablations several times and succeeded in delaying systematic treatment. Nothing is totally curative. It's all about kicking the can down the road and it's working for me

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How could you possibly know that? Progression is known to be very slow at first anyway.

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Because I was a gleason 9. The slow part followed surgery in 2005. Did worthless radiation in 2010 and watched my psa doubling time change from then on. I have now had a lot of different treatments but keep finding ways to bring my psa back down and kick the can.

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Treating PSA is not the same as treating the cancer.

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True, but outside of scans, what else do u suggest for continuous monitoring?

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It's not a matter of continuous monitoring. MDT can only be proven in a randomized trial in which SURVIVAL is improved by the therapy. The CORE RCT in the UK will have overall survival as an outcome. It may be possible to use circulating tumor cells (CTC) as a surrogate endpoint someday, but such use has not been validated.

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Thanks, MDT=?DurableTherapy?

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Sorry. MDT=Metastasis-Directed Therapy

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Well you can only prove that it IS effective or that it IS NOT effective in a properly constructed trail. But if medicine means only dispensing what is proven to work for the exact class of people that match the trial population, there is not much need for a doctor. A computer could do it. I don't mean to justify doing "whatever you feel like", but there is room for experience and hunches.

As for CTC's, prostate cancer cells in the blood have undergone EMT one imagines. Does that make them fall into the "stem cell" category, or are those two overlapping categories, or distinct categories? Certainly being able to kill all CTCs in the blood seems like a handy thing to know how to do.

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I have nothing against MDT when it is safe to do, and when the patient does not forego systemic treatment while getting it.

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Thank you, what do you think about the PS MA scans being slightly more accurate?

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They aren't slightly more accurate, they are much more accurate.

pcnrv.blogspot.com/2016/12/...

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Much more accurate than the T99 scans, and that has been known for a long time, yet T99 is still the scan that "everybody" gets. Shake your head if you will.

The question was in the context of the various other scans. Are they (the PSMA small molecule ligand scans) "much more accurate" than the other scans, excluding T99?

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Read the article for the answer - that's why I posted it.

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I did. The article is about T99! Technetium. Quote from the intro:

"The traditional way of finding distant metastases is to use a technetium bone scan"

But your answer could easily be taken to mean that the PSMA scans are "much more accurate" than the C11 scans and the aux scans and the Fluorine scans.

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I hope you will read beyond the first sentence.

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Yes it's a nice article, but it does not say that a "PSMA" scan is "much more accurate" than F18-DCFPyL.

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You are confused. DCFPyL IS a PSMA scan

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Which type of scan, or which type of PSMA scan, would best help predict a skeletal related event, or signal that treatment was needed to prevent serious compromise to the spine?

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A CT scan.

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A CT scan (x-ray) not a PET (positron)?

Yup, I am confused. I didn't expect that answer.

I have reacted to contrast, so CT with contrast is out, at least the Iodine class.

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They always do a PET and CT scan together because a CT scan is MUCH better at finding the geographic location of the bone mets, and showing details of the kind of bone damage you are asking about. A PET scan only identifies where the mets are, not what the bone damage is.

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Ah. Thanks.

Is it that the CT shows the bone, such as it is,

whereas the PET lights up the prostate cells?

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No, PETs do not detect healthy prostate cells. Read the link i provided - it explains what they all do.

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Well a prostate cell in the bone would not be healthy, by definition.

My question, such as it was, implied that there might be other tissue in the area of interest beside 1) bone and 2) cancer prostate cells.

And if one was interested in the bone in particular, to assess its shape although not its strength, that you were saying that the CT would be the test to use, because to assume that there was bone wherever there was not tumor would be incorrect.

I was, I thought, restating what I thought your logic was.

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Slightly more accurate than what, exactly, did you mean?

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OK let me share a little more information with you guys. I appreciate all of you. And I’d like your opinion on next steps. 10 years ago , Age 50, my prostate cancer was discovered.I had a Gleason score 4+4. Underwent radical prostatectomy, and salvage radiation therapy but the PSA never declined below 0.7. Followed in years two through five with IADT and watchful waiting but steady increase in the PSA to 10. It finally went on Lupron permanently in years six through eight. PSA stayed below one until within a six-month. It increased to 236. Years nine and 10, I have been on Zytiga that dropped down the PSA once again 0.8. Only recently has it begun to rise. When the PSA reached 14, I participated and the testosterone BAT trial at Johns Hopkins. I was encouraged because I had a check2 mutation and Dr. Denmeade MD thought that my PSA would calm down. Unfortunately it rose from 14 to 92 at which point I have elected to see Dr. Kwon on June 6. I have no problem with pin point or systemic treatment. Nor do I fear radiation or surgery to remove suspect lymph nodes or metastatic disease. It has not been easy dealing. Not having testosterone has been a real struggle for me but I get up and exercise every day and try to watch what I eat.

I’m definitely running out of bullets in my gun! Just thought I’d share it with the group any comments or thoughts are appreciated :-)

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Me too. Or at least similar. PSA rising from 2 to 4. To hopkins for BAT. PSA rose to 50. Bailed. PSA continued on up to 70 then falling. Went to Rochester. Saw Kwon, hoping to get into a trial for oglio there. The scan showed I was beyond the oglio state so that was at least a clarifying insight. My appointment was at 8 AM. I was there at 6:40 and so was Kwon. Most of the lights were still off in the waiting area, and no schedulers were at the desk stations. He gave me the standard suggestions for treatment, plus also Heidelberg Germany where they are doing the 177Lu-PSMA-619. My doctors here in Buffalo are all "Let's wait and see". We don't want to fire a gun now that we may need later. (huh?)

The only thing is that if I start with 177Lu that will certainly exclude me from the coming 225Ac trials.

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And one more thing, why last CAT scan shows metastatic disease in the , retroperitoneal, obturator and one external iliac lymph gland

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It would appear the only reason you would consider MDT at this point is if the scan (11C Choline, Auxim, ga PSMA) would show concentrated metastasis in a few places that could be removed by radiation or surgery. However, you clearly have systemic disease and I would suspect any delay in the next systemic treatment would be short lived at best. When I get to the point you are at now, I would not consider MDT for that reason. I would look at second line antiandrogens (enzalutamide, apalutamide and daralutamide), or the new Lutetium 177 radiation treatment. Or go for less is more and take a few bicalutamide pills just for the fun of it and see what happens.

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would you take bicalutimide even if for T less than 5?

To interfere with adrenal androgens??

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I personally would not take bicalutamide if my PSA were as low as 5 (even though it could block the androgens from the adrenal glands) unless the scans or some other information showed metastasis. Unless you have the type of PCa that produces very little PSA, it is unlikely that a PSA of 5 or less is life threatening. But that's just my perspective because I started out with a PSA of 136. I see no reason to treat very low PSA with ADT and potentially cause castration resistance. I acknowledge my viewpoint is in the minority and outside NCCN guidelines for recurrent disease.

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I should have said "outside the NCCN guidelines if there are symptoms or progression shown on scans". "Observation" after recurrence is still a NCCN choice of "treatment". See NCCN Clinical Practice Guidelines Version 2.2018.

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The question was T<5, not PSA<5. If your testosterone was very low, would you still want to block the adrenal androgens?

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Sorry. Need better reading glasses. A T of 5 is considered castrate with the goal to get it under 20. But if your PSA nadir is not as low as you want it to be with a T of 5 and you are only using a standard LHRH agonist or antagonist (eg lupron or firmagon) which reduce T generated by the testicles you could add bicalutamide to block androgens coming from the adrenals. Some would recommend adding an AR-5 inhibitor like finasteride or dutasteride (which lowers DHT) for complete androgen blockade. If your PSA is already ultra low with a T of 5 I would question why there would be a need for the additional agents.

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No it's not. T is low, but PSA is not low.

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As Ed McMahon used to ask; "How low is it"?

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At the moment, it is 10, but I am in the "washout" period after a BAT treatment. Falling from 70. Who knows what it means.

The doctors say that that is "good", but that just makes me think that they don't feel like thinking: satisfied with superficiality.

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So back to your original question about adding bicalutamide. If you are on BAT, then you are already castration resistant. You are in unchartered territory about how adding bicalutamide will affect this new protocol. The question is how does androgen reception and signalling become hormone naive after receiving high dose testosterone, assuming that is what happens on BAT. I like the BAT theory. It supports my IADT theory of using low dose bicalutamide. By not completely depriving the PCa cells of androgens during the on period, the cells do not have to look elsewhere or from within to find other sources of androgens for sustenance. Then, because bicalutamide blocks androgen receptors, more T circulates in the blood stream, to the extent that it doubles. When the off period begins, there is lots of T to "refresh" the PCa cells, thereby keeping them hormone sensitive - like mini-BAT. My theory is all unproven, unscientifically based supposition of course.

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Just got my latest PSA after going off of testosterone BAT trial. It is at 73 down from 91. Holding off calling back on the Zytiga until I see Kwon.

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I found my PSA fell (post BAT) at a little slower rate than it fell on initial ADT treatment. I had not thought about that when I decided to apply for the BAT trial. The post-trail "washout" period is pretty long. It means you can't join another trial until you get back into some more common biological state. If you join a trial with your PSA falling, what is the PI to make of your numbers? Was it an effect of the trial treatment, or an effect of coming off the prior treatment?

Please say "hello" to Kwon from one of his many anonymous admirers.

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I will !

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Hey guys I appreciate all of your comments even the ones that can make me pretty sad. I’m feeling pretty beat up right now since Zytiga stopped working for me which is why I went on the BAT study I get it regarding the difference between the choline scan and the PSMA scan. I’m a little down because now that I am post BAT, JHH wants me to go back on the Zytiga but I want to see what Kwon can do.

Outside of seeing if we can get a little more mileage out of this IT guy, then all I have left to hope for is some immunogenic drug that will push back on the cancer because of my c outside of seeing if we can get a little more mileage out of Zytiga , then all I have left to hope for is some immunogenic drug that will push back on the cancer because of my chek2 mutation.

I’ve been battling this thing for 10 years but this is the first time im feeling that I’m not winning the battle anymore. Anyway just how I feel thanks for your comments.

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