Under 50 - 3 Years out with M1b disease - an update!

[AlooGobi]

It’s been a trip but I want to say thank you to all you guys out there for some really incredibly insightful and encouraging posts over the last 3 years I check in monthly and think this is a wonderful resource.

My own story started with a relatively low PSA 3 years ago of bouncing around 3 with 3 bone mets spine + hips and after much research and discussion, elected to have a comprehensive kitchen sink treatment of adt / Docetaxel / RP followed by SBRT to the 3 mets all within 6 months of dx.

My PSA went to undetectable during month 4 somewhere after my first or second taxotere session. My T dropped to below .2 quite quickly as well. I had negative margins and extended pelvic lymph dissection at surgery with negative nodes.

I stayed on ADT for 15 months tip to tail and was scanned using MRI and Pet every 6 months regardless of the undetectable PSA.

I stopped ADT in September 2019, had full T back within 5 months, and was undetectable with full T for approximately a year.

PSA rise in March of this year of .24 brought me to a quick PSMa pet where the visualized met was blasted with 18gy in one session.

Out of an abundance of caution, my care team did a number of labs to rule out neuroendocrine and thoroughly hunted for any other mets using other tracers as well as traditional imaging. No other uptake or mets.

The radiation was painless, quick, and I got to choose my Spotify mix during the session. The toxicities of SBRT compared to standard of care are quite good, and with the dozens of papers on Google Scholar on this, i suspect anyone who steers people away from SBRT and pounds the table for systemic therapy just is a rogue agent paid by Janssen.

Like Break60 and a few other guys on here, my particular care team has sold me on the value of metastasis directed therapy for macro cancer, although I recognize it’s not curative by itself. Seems like zapping a met is ok / and zapping all mets seen by PSMa is better and really does make a difference as far as progression. But dealing with micro disease as well as the macro seems to make a real difference as far as progression. No overall survival data yet, but aren’t we all just buying time till they figure out immuno for this anyway?

A few months out, PSA is back down to undetectable and on the basis of progression free survival time for any studies out there looking at “concomitant” ADT, I’m ok with going back on Lupron and Xtandi for a while - length tbd.

In my own personal situation, on the hundreds of hours of research I’ve done, I believe this is the best course of action for me.

The reality is that anyone who pursues metastasis directed therapy as a form of tumor management is playing roulette with a hypothesis whose data has not matured sufficiently to make a compelling argument for long term survival benefits.

But when I punted this point to a global leader in the field (top institution, h-index of 100+) - he basically said - look YOU are the data set. I don’t have 10 year survival data because we’ve only really been doing this for 5 years. But I can tell you this - for low volume metastatic guys, let’s say I have 70 of them, almost all are alive at 5 years and the majority of them still castrate sensitive- so go ahead and compare that to the standard of care. And yes I know Stampede OS is compelling for the low mets subgroup, but staying castrate sensitive at 5 years as a group is surely a nice point of differentiation. I remember when I started on here, some of our in house scholars were declaring “there’s no evidence whatsoever that treating the primary helps at all in M1 disease”, which basically most oncologists at the Mayos and MDs and JHH and Martini Klondike of the world would tell you by now is nuts

On a personal note, I drink the seed to soil kool-aid, as well “whole person” naturopath philosophies, have a nice bag of my own supplements, believe in visualized meditation, hypnotherapy, acupuncture, the endocannabinoid system, Dr. Moss, New German Medicine, the placebo effect, and a bunch of other things too weird to mention.

I’m happy to serve as a resource, particularly to any around or under 50 year olds freaking out and looking for a peer in the age group to kibitz with.

Cheers.

[Schwah]

My situation is very close to yours. I had 3 mets 8 years after focal Chryo surgery and hit it with SBRT/Taxotere/Lupron m/Zytega for 21 months to undetectable. All my scans showed no residual cancer in my remaining 60% of a healthy prostate. 15 months into my ”vacation” I found one small met (on my every 6 month PSMA SCAN) on L-5 which I just finished ablating with SBRT. I now deciding whether or not to go back on another round of Lupron/Adt for 6-12 months. I did one other thing that’s kinda crazy. I’m in the midst of a 3 round infusion of Provenge. Insurance does not cover it because I’m still hormone sensitive so the cost is stupid high but my wife and I decided to invest in my health. Provenge studies all seem to show that like most treatments, the earlier you use, the better the results. And there appears to be a synergetic effect when combined with ADT and with SBRT.

Im not clear if you plan on another round of ADT or not. You say your doctor has 70 some odd guys doing metastic directed SBRT for 5 or so years and most are still castrate sensitive. My doctors at ucla say something similar. My question for you is are all or most of his 70 also doing ADT/Zytega or ADT/Xtandi? Or are they using SBRT as their sole treatment hoping that way to stay hormone sensitive longer that way? And what is your latest thinking on going back in systemic treatment?

Schwah

[MateoBeach in reply to Schwah]

Yes, Schwah, I too am not clear on his ADT plan going forward. Perhaps short term - 6 months adjuvant when met(s) treated with SBRT? I'm in the same general boat. Off ADT for over a year since PLN RT for 2 nodes. Getting another PSMA scan next month (PSA 0.18).Good for you for ponying up for the Provenge. I'm convinced it does good things and prefer it early, as in HSPC. Out of pocket for it is tough for anyone, and out of reach for so many.

[Schwah in reply to MateoBeach]

I just read your history Mateo. Interesting. You too appear very proactive in your treatment. Congratulations on that!!

So you were on an early hormone sensitive Provenge trial as I understand it? Correct? And that appeared to provide no meaningful benefits? I’d really like some more information on that trial if you have anything? Did you ever do the LUPSMA Treatment in Australia?

Schwah

[MateoBeach in reply to Schwah]

I cannot say the Provenge provided me no benefit. I just cannot quantify it since it does not lower PSA. But I am still here and still HSPC 10 years later. And no Mets on scans outside my pelvis. Would get a booster if I could.

[Schwah in reply to MateoBeach]

Good point. Is there any info on the trial results out there ??

[MateoBeach in reply to Schwah]

It was a study to compare the T cell markers of immunity from Provenge started before beginning ADT vs while already on it. It was not to follow clinical outcomes. There was not a significant difference so they did not pursue a trial to get it authorized for use prior to ADT.But it appears Provenge works. Better when given in earlier, less advanced disease. So the lack of approval for HSPC is a “rat-f@#k” IMO.

[AlooGobi in reply to Schwah]

Hi Schwah! I think if you put 10 top oncs in a room who (caveat) were believers in MDT, you'd get 5 different opinions as to length and type of ADT. In this particular conversation, TopOnc says something along the lines of "if a guy has the capacity, emotionally and financially, it has become my strong preference to do MDT, and repeat MDT without ADT, if i'm using PSMA + traditional imaging..." Now this was the extreme minority position in my consult journey - but an interesting one to consider... for me, I thought the data for PFS was too good with concomitant systemic therapy (usually the most compelling p-value among the dozen or so papers looking at this, meaning guys who ablated mets consolidatively with some sort of intermittent or short course systemic therapy did a lot better than guys who just treated the mets (mas o menos 9 months pfs vs 20 months pfs)...

Now what I thought was the most interesting is that, outside the interquartile range for data sets that report the full cohort, you get a good, albeit small, double digit % of guys who don't seem to progress after MDT - not the ones that aren't censored but those who somehow chug along now after 2 or 3 years without any progression. Annoyingly, you get a mirror-like 20-25% on the other side who get MDT then show up polymetastatic and in terrible shape, for whom staying on the drugs may have made a much better difference. The most interesting bit about all this is that Germans and Belgians and the Dutch have been playing with this for a good while longer (even with PSMA scans!) than in America, so there's single-institution data out there with much longer time frames.

[On the other hand, you have ARCHES and TITAN that basically say combined blockade low volume mets guys do better anyway (and can postulate that we really don't know how much SBRT helped) or people that posit that 'well you're just treating PSA...' But the ablative potential of lasers to blast almost all cell lines in a met is sort of like nice wide margin surgery taking out treatment induced clones that were baking after neoadjuvant chemo before they have a chance to seed...same idea...you're ablating tumors that may have, among them, cell lines that may not respond to treatment with certain systemic therapies, or may develop/morph because of those systemic therapies...]

[Schwah in reply to AlooGobi]

Great response with obviously no clear answer....lol. You’ve done a lot of great research on this subject so thank you for sharing.

Let me add one thing to the mix that became pretty clear to me from my research and specifically with my conversations with the UCLA radiologists doing this a lot. They truly believe in the abscopal affect being that the ablated mets actually spark the immune system to go after other micromets unseen in the scans. Killer t-cells have bern consistently shown to increase substantially in the months following MDT. Here an interesting study

clinical-genitourinary-canc...

This thinking about getting my own immune system working for is what led me to Provenge (Sipuleucel-T) and my plan to follow up with ADT . “Sipuleucel-T→ADT appears to induce greater antitumor immune responses than the reverse sequence.” The thinking at ucla is that ADT also has a synergetic impact with MDT.

If you don’t mind I’d appreciate a few clarifications on your reply:

1. Who or what is “TopOnc”. I’ve never heard that expression.

2. TopOnc preference for no ADT was subject to ongoing PSMA scans plus “traditional imaging”. Why the need for adding traditional imaging. I had a number of conversations with Dr. Czernin who runs to nuclear medicine and PSMA scanning at ucla and he was quite clear that the Pet Scan portion of the PSMA scans should pick up and non PSA avid lesions as well or better than other scans so no need for any other scans.

3. In your discussion on the mirror image interquartiles of the “very good” and “very bad” results, we’re both the groups of people who were not doing concomitant systemic treatment? If so, were there similar stats for those doing concomitant systemic treatment?

4. You mention the Europeans who’ve been doing this much longer with stats from single institutions ? Do you have access to those stats or perhaps any mets analysis on them?

Again good work on your own research and treatment. What’s the odds you will add the ADT for yourself?

Schwah

[AlooGobi in reply to Schwah]

1. I made it up. Important guy who does conferences and tons of research.

2. For non PSMa avid lesions (yes such a thing), especially with low PSA, concern for small cell and/or neuroendocrine a thing - use of FDG pet can possibly pick up those mets that PSMa could miss. Very rare. Czernin is a genius. Love watching his talks on YouTube. FDG basically would ALSO confirm a non PSMa avid pet finding OR also tell you if your mets are FDG avid if you don’t have access to PSMa. Or even if you get a PSMa, you can do an FDG pet to answer the question “let’s see if FDG also picks them up” if that’s what you have available at home.

3 + 4 - Single institution studies on Google scholar - not phase 3 - they could all be lying 😉 who knows! But toss your search terms into Google scholar PSMa SBRT PFS and you’ll get 10-20 articles over past 5 years. I think most of the studies were not doing concomitant adt but there are some very specific concomitant adt vs no adt studies that demonstrate superiority of adt. Now if you compare intermittent adt alone without SBRT - I think the data is like 8 months pfs. And if you look at SBRT alone, the data is similar - 8 or 9 months pfs.

Finally, I myself added ADT and Enza. But I like Klotz’ research out of Canada on intermittent adt and the other single paper out there (again, terrible single institution, probably used terrible methods, or they were Italian or whatever) on non-inferiority on intermittent enzalutamide in a bcr setting with no mets on traditional imaging where a 3 month course of Enza got these guys a remarkably good pfs - with the top ten or fifteen percent in excess of a year…now they didn’t have mets on traditional imaging, fair, but based on the number of guys that are upstaged using PSMa, you can bet a large whack of them would have, had they.

So for me, sort of stacking as powerfully as I can, it’s intermittent adt plus intermittent Enza plus SBRT. Obviously my justification for this is purely hypothetical and I’m not a doctor etc etc etc …

[AlooGobi in reply to Schwah]

Oh and fwiw, I think that UCLA is outstanding and you’re lucky to be treated there. It seems like the collaboration between medical oncology and radiation oncology and surgery there is quite strong - czernin, calais, kishan, drakaki - all sort of doing work together in the same space on the same page and not so much the my way or the highway approach. I really like the oncs that are open and chatty on Twitter. You can learn a ton!

[Hidden]

In an earlier post you were hunting for an MO. Where did you land?

[MateoBeach]

Great plan and execution AG. I endorse and admire your progressive all-in style. Am on a similar path. Dx at 57- RARP, Docetaxel and SRT that same year. Now 13 years later I am still hormone sensitive. PSMA scan showed only 2 PLNs about 15 months ago. Treated those (hemipelvic) nodes with "boost" and 6 months of ADT(well 5 anyway!). Just completed a 1-month personal trial of high dose testosterone to restore my withered body. PSA behaved well, mildly up, then down again, but not undetectable. Now 0.180 (off of all meds). Going for a repeat PSMA scan next month.My inclination (not supported by trials) would be to do short term (6 mo) adjuvant ADT with SBRT for any new oligomets that pop up. As long as PSA stays low. And add in one month of high (SPT) testosterone every 4 to 6 months when off it. Seems similar situation to BCR (micrometastatic) disease situation where early start of continuous ADT vs delayed is not yet clearly resolved.

It may not be logical, but I fear that going on continuous will start me on the death-spiral towards castrate resistant disease.

It is great to have your perspective and clear writing here, AlooGobi.

[AlooGobi in reply to MateoBeach]

Thank you for the kind words! I’m also not too clear on my ADT plan going forward, but we didn’t love the kinetics upon the bcr so the plan, for now, is to add combined androgen blockade to SBRT for a while, go off, scan and labs, and hope for the best. (I realize the alternate approach of continuous ADT and Enza has some merit as well - a few nice papers where a guy can pop up with a few mets that are resistant to combined androgen blockade, hit the mets with SBRT, and then go back down to undetectable - the idea being since “cancer is a heterogeneous disease” that the agonist/antagonists are still working on their respective lines)

There are decent studies, which I’m sure you know, that suggest that any concomitant ADT period alongside SBRT in excess of 6 months makes a difference in progression. A number of MDT papers in 2020-2021 are hypothesizing / concluding with language to the extent of “I think the next step is to combine intermittent ADT and SBRT” … my RadOnc says this has evolved to become his standard practice, with a wink “you want to wait 10 years for the data to mature before we do this?”

You know what’s really reassuring to me - when you think of all the guys in the pre PSMa era who had bcr and were deemed non metastatic - put on hormones for a while and given radiation to the bed or fossa - and then taken off ADT - that both a significant number of them were long term survivors ANd that in 2021 a number of them would have likely been upstaged to M1 with PSMA imaging.

And Mateo, your profile is inspiring! You’ve hacked your way through the weeds for 13 years with a similar temperament, I think, to my own. Would be thrilled as well to hear about your psilocybin journey // my consulting psycho-oncologist is a huge proponent of a macro journey - I wonder if the synergistic effect of the serotonin wave that accompanies such journeys would have a similar modestly beneficial effect as the studies on concomitant anti depressants seem to be suggesting.

[Schwah in reply to AlooGobi]

One more clarification AlooGobi. You say “...any concomitant ADT period alongside SBRT in excess of 6 months makes a difference in progression.” So are you saying less than 5 months may not be beneficial? And what seems to be the consensus of the ideal length of time and how long do you plan on going ?

Schwah

[AlooGobi in reply to Schwah]

There’s a paper out there that measured time to progression post SBRT and found that concomitant adt of less than six months to be equivalent to no adt.

I don’t believe they did a subgroup analysis for second line (enza, abbi, or apa) or combined androgen blockade, though, and it was retrospective analysis which puts the quality of the data under greater scrutiny.

[Schwah in reply to AlooGobi]

So whats the consensus on the time frame of ADT from the guys you’ve spoken to and how long are you gonna go with?

Schwah

[AlooGobi in reply to Schwah]

I have 3 different oncs I work with saying 6, 12, and 18. Just started. Not making the decision about 12 or 18 till I hit 6. So many variables and small studies keep trickling in.

[Schwah in reply to AlooGobi]

I have 2 I work with so let’s stay in touch and compare notes. I would think the timing might be related to hitting undetectable PSA and staying there fir some period. Did that come up in your discussions? I would love to hear Tall Allen chime in on the subject...

Schwah

[AlooGobi in reply to AlooGobi]

But what I’m doing for which there is little to no data is combined androgen blockade with Enza plus SBRT. So it’s dealing with both macro and micro disease, and I have my Google alerts set for intermittent Oligometastatic.

The one sort of scary bit is that there are some guys on here that cruise on adt for many, many years - and I wonder would they have been worse off had they stopped, especially with undetectable psa values - the foot keeps the beast down.

Equally, there are profiles where guys have a real hard time with the comorbidities of adt and have managed their disease more aggressively almost expecting mets to come back and treating as they come.

But that’s where these sub-group analyses are important. One study said that the most relevant factor for distant metastatic recurrence was psa-doubling time - which kind of makes sense - if you’re ablating macro mets but the micro mets are freaking out super quick, you’re probably going to end up in that unfavourable group.

Then there were another few interesting papers where guy was on dual androgen blockade with Enza, and sprouted a met- psa went up- but the one SBRT brought it back down to undetectable for the next year (they stopped following after for the purposes of the paper)- assumption made that adt keeps those adt mets down, Enza keeps those Enza mets down, and in this case, SBRT dealt with the rogue met before it went nuts and cloned off a bunch.

So that’s what makes it more complicated, right? It’s pretty clear now that stacking treatments to deal with all cell lines results in much better control and 5 year survival for m1 guys- but they haven’t been doing it long enough to know what happens next - what if all the treatments stop working at the same time?

So some docs are like let’s keep you on hormones forever and deal with mets as they come and hopefully the added SBRT will make that top 15% long term survivor number better.

Other guys posit that we know the vast majority burn out - so let’s do gas on / gas off for as long as we can- meaning until and if you show up polymetastatic - and we think using super sensitive scans and aggressively monitoring for weeds in your garden will get a larger number of guys better outcomes.

Point being, nobody knows. Every doc is different. But when you actually do a deep dive into long term survivors, you can see they stack more than treatments - they stack lifestyle changes, attitude, the (placebo) mind body connection, stress level control, all of it. Read the book Radical Remission, it’s fantastic.

[LearnAll]

Enjoyed reading your descriptive post. But Aloo should be less and Gobi should be more along with a lot of masala😀 Best wishes.

[pjoshea13 in reply to LearnAll]

It's all carbs of course, but a very comforting side-dish.

indianhealthyrecipes.com/al...

-Patrick

[LearnAll in reply to pjoshea13]

I can assure you that I am able to make even better tasting Aloo Gobi myself. Just finished dinner,,,with Bhindi Masala (spicy Okra) ..loaded with Glutathione ,fiber and senolytic chemicals . Okra plants are growing well in my backyard. Next month will be good crop. You are invited.

BTW..I read today German papers about Senolytics (Quercetin, Fisetin, longpiperine etc) I noticed that my diet has good amount of senolytic substances.

And the discovery of ATRARIC Acid, a chemical found in African tree bark (Pygeum africanus) which contains anti androgen which does not become agonist with time.

In Germany, they are trying to make an anti androgen drug formulation out of this bark.

Can't believe I found the Pygeum bark on Amazon.. ordered some just now.

pubmed.ncbi.nlm.nih.gov/209...

[pjoshea13 in reply to LearnAll]

Pygeum A. has long been a common supplement for prostate health. Many products contain it. Mostly used by those with BPH. Often with saw palmetto. Unfortunately, a lot of these products are not standardized and may not even have the desired sterols.

-Patrick

[LearnAll in reply to pjoshea13]

The paper by The article "A natural Androgen Receptor Antagonist induces cellular Senescence in prostate cancer cells" . It concludes by saying Atratic Acid (in the bark) inhibits multiple paths which may be promising in tumor growth inhibition." So seems the benefits go beyond just treatment of BPH. Will keep an eye on it.

[pjoshea13 in reply to LearnAll]

This full-text paper is a bit older:

The natural compound atraric acid is an antagonist of the human androgen receptor inhibiting cellular invasiveness and prostate cancer cell growth

ncbi.nlm.nih.gov/pmc/articl...

You might find this 2019 study to be if interest:

Chemical comparison of Prunus africana bark and pygeum products marketed for prostate health

"The bark of Prunus africana may contain atranorin, atraric acid, beta-sitosterol and its esters, ferulic acid and its esters, and N-butylbenzene sulfonamide, compounds that have been shown to improve the conditions of benign prostatic hyperplasia, enlarged prostate." ...

pubmed.ncbi.nlm.nih.gov/303...

Note:

"The amounts per gram of the BPH-active compounds atranorin, atraric acid, total ferulic acid, and total beta-sitosterol and the fractions of free beta-sitosterol were quite different in bark from Prunus africana and in the contents of commercial pygeum capsules, contents purported to be derivatives of the same bark. This was unexpected and suggested that the BPH-active components in com- mercial pygeum may not be fully sourced from natural materials as labeled."

sci-hub.do/10.1016/j.jpba.2...

-Patrick

[Spyder54]

AlooGobi, a great Mothers Day morning read. Thank you for sharing. I was just turned down by the SWOG 1802 study at MD Anderson because of fluctuating PSA & Testost levels. They think my Cast Sensitive may soon become Cast Resistant. SWOG 1802 is trying to prove with 1200 men in a Phase III Trial that what you have experienced thus far may become a New SOC for Oligometastatic PCaQuestion: Where are you being treated? Do you recommend your URO/MO Team?

Thanks,

Mike K

St Petersburg, FL

[AlooGobi in reply to Spyder54]

Hello friend! I combined Mayo and Hopkins. Great high volume surgeons there - Hopkins - Pavlovich (and Tran for RO ) + Mayo - Karnes (and Phillips - (former Hopkins guy) and Stish) - all these guys generally on the younger side - bit of a different crew than the older "we go to Davos every year" drug company guys - but all the younger guys are all on twitter with open accounts and they real-time share their own data / stories / abstracts ahead of the big conferences.

[Spyder54]

Thanks! I noticed 3 yrs ago you also posted Ken Pienta at Hopkins. Still working with him?

[AlooGobi in reply to Spyder54]

He’s great - obviously springboarded off his own TED protocol - basically the same thing as the SWOG 1802- but just consulted with him.

I think he’s a genius and I appreciate his creativity. In a few talks you can find online, he acknowledges making moves like sending castrate sensitive early days guys to Baum at Heidelberg at the earliest days of Lu-177… really has his patient’s best interests at heart and I think he practices a few moves ahead and doesn’t keep a large cohort of his own patients.

(You know, Pienta was the guy who back when he was in Michigan, came up with modified citrus pectin as a thing that helps inhibit mets…)

[Hidden]

Nice Post and sorry you are going through this at such a young age.

Are you still working? I am but I do notice after nearly 2 yrs of ADT+zytiga I don't have the stamina i did before this pca journey. For me, diagnosed at 53 in May 2019...RRP in June 2019 and adt in July 2019. The IMRT in oct 2019 and zytiga in nov 2019.

Best of luck to you.

[Muffin2019]

You give great inspiration and hope to all of us, keep the posts coming.

[Hidden]

My hat off to you young men in their 40 and 50s. I was 53 upon dx myself . I’d bet that the year with full t and no PSA felt great ! I’ve been on adt full time six years. No t . Personally my belief is that for those in their 50s or even in the 40s that pc is an entirely different ball of wax. Taken down in our prime earning years . Cut short in all

Aspects . Hang in there. Great job encouraging others .💪🌵

[Hidden in reply to Hidden]

Lulu...

I sent you a private message.

Had a question for you.

Cheers

[AlooGobi in reply to Hidden]

Like few others on here, I suffered from hormonal imbalance since childhood, was diagnosed with hypothyroid in my early 20’s, and had baseline upper limit testosterone, lived quite sluggishly- strangely enough, found a greater sense of stasis and felt less sluggish while ON ADT.. (does anyone know enough about hormonal imbalance to unpack this for me?). I know it’s bizarre but so is getting m1b disease in 40s with no DNA defects or history of cancer in family. 🤷🏻‍♂️

[Hidden in reply to AlooGobi]

My dad had pc .Yours is a real conundrum..I’ve never heard of that before., from the early 20’s . I’m sorry , that

Must have sucked for you? I was was pretty normal until my forties when I slowed down a bit .. Maybe I had low t. Never had it checked ..🧐

[j-o-h-n]

TO ALL,

I must admit what I tell people when they're talking to me and I'm not wearing my hearing aids. I tell them "If I'm smiling and nodding my head yes, that means I haven't understood a fucking word they said". That's how I feel reading this post.....

Good Luck, Good Health and Good Humor.

j-o-h-n Monday 05/10/2021 7:24 PM DSTa

[Hidden in reply to j-o-h-n]

That's okay j-o-h-n...for you we have choc chip ice cream(2 scoops) , a box of munchkins (stale like you) and a bib to catch the drool.

[j-o-h-n in reply to Hidden]

The best part is the drool...........

Good Luck, Good Health and Good Humor.

j-o-h-n Monday 05/10/2021 10:38 PM DST

[Hidden in reply to Hidden]

😂😂😂dam that is cruel

[Hidden in reply to j-o-h-n]

As we smile and nod at your comments as well.😷

[Boywonder56 in reply to j-o-h-n]

Couldnt have said it better myself......makes me feel inadequate....but since adt im used to iy

[Spyder54]

AlooGobi,Wow! We must drink the same Kool-Aid. I read, in my first month of Dx, from a Harvard Med post regarding a Sloan Kettering Memorial study of 20 Men who did your similar path, with similar outcomes. I believe in the “Abscopel Effect”. But first you have to get there. I am 67 and 8 mos since Dx. My PSA has been slow to Nadir. Just now down to 2.2 (where you presented low, I presented high at 47). I too am Oligometastaic. Trying to find a Surgeon for RRP has been a challenge, but waiting for that first low Nadir is probably key to hit the PCa while in slumber (senescence). Now! Meeting with a well known Surgeon, with over 2,000 under his belt, this week to hopefully schedule. Follow up with whole pelvic Radiation, 6 courses of Docetaxel, SABR any found Bone Mets, and top off with an additional 6 mos (tbd) of Current Lupron, Zytiga/pred, and a host of supplements, all while keeping up my morning visual meditation, blessings, yoga, mobility, dumbells, plant based diet. As You and Schwah have said….Throw everything at it, including the kitchen sink, and early is better than later. Create an environment no PCa cells would want to reside in. Please keep us posted. Gosh we hope this extends OS. As you said, these are early chapters. Early times.

Our best to you and yours,

Mike

St Pete