My Gleason 3 + 3 Prostate Cancer Is Now Metastatic

In February 2011, I was diagnosed with Gleason 3 + 3 prostate cancer with only 10% of 2 cores out of 12 was cancerous. I had brachytherapy in June 2011. My PSA dropped quite rapidly to 0.1 from pre-biopsy value of 3.4 within 2 years. Then in 2015 it started rising reaching 1.5 by July 2016. A biopsy found an extra-capsular cancerous nodule. ADT between October 2016 and April 2017 and cyberknife in January 2017 treated the recurrence. My PSA remained undetectable from April 2017 to January 2018. Then it started to rise quite rapidly: April 4: 0.2, July 13: 0.9, August 28: 1.3, October 4: 1.8, October 22: 3.26. The last PSA was just before a 3T MRI and 18F-DCFPyL PET/CT scan under a clinical study. The MRI didn't detect anything significant, but the PET/CT scan detected cancer in several lymph nodes in the pelvic region. It shows how sensitive the 18F-DCFPyL PET/CT scan is. This scan is yet to be approved by FDA.

I know some people will respond saying that a Gleason 3 + 3 cancer does not become metastatic. I am not going to argue for or against that. The bottom line is that I have metastatic cancer, a journey that started as Gleason 3 + 3 diagnosis 7 years ago.

Going,
Very sorry to hear that. Do you have a plan for going forward?

For you—for your case, since you decided to seek treatment—it is entirely moot to question whether a cancer originally diagnosed as Gleason 3+3 later also grew a more aggressive version of PC and went metastatic or not. For you, it’s only a question of whether your treatment was a success or not. I’m sorry to hear that it wasn’t.

If you were diagnosed today, at a minimum you would have sent your original biopsy samples out for 2nd opinion on the pathology, then had a follow-up, confirmatory biopsy within about a year to decide whether to start on an AS program…I suspect that one of those two things would have led to treatment.

It turns out that only about 2% of men diagnosed initially with low-risk PC eventually grow a metastatic cancer...and this percentage is essentially the same whether they seek initial treatment or start initially on AS. Nobody said that treatment stops all failures, and nobody said AS prevents all failures either...although the data shows that the failure rate is the SAME whether the men seek immediate treatment or not.

What's the plan for the lymph nodes? Finding a surgeon to attempt removal of a radiated prostate may be difficult.

Post Edited (Blackjack) : 10/26/2018 1:52:46 PM (GMT-6)

Man, I'm so sorry to hear this. Do you have a good MO at this point? Hoping you can treat this as a chronic condition for 10+ years, although I know this is not the news you wanted to hear.

While my PCa history is not the same as yours I kinda ended up in the same place. I also had a 18F-DCFPyL PET/CT that indicated lymph node activity. I then had SBRT to those lymph nodes as a part of the ORIOLE clinical trial at Johns Hopkins. My PSA dropped from 3.6 to 0.3 over the past year and a half and is holding a 0.3. A second 18F-DCFPyL PET/CT showed the lymph nodes clear of cancer. Click on the "VIEW IMAGE" below for more details.

...Jerry

So sorry to hear this news, I hope that you keep us updated with your treatment plans. Please stay positive and do not give up as you have a great support group right here. Prayers sent your way for a cure.

What is your age now and do you maintain \hope that at your advancing age you will not die from Pca...and will most likely live into your 90's doing nothing...I assume you are healthy as can be if you do not include Pca in the mix...enjoy your future years...don't weaken now...and do a header into the reef....

That sure is a kick in the teeth. It does point out, as others have said, that biopsies are not all that definitive of the true situation. After all, as we often point out in here, a significant percentage of surgery patients have an upgrade when the whole gland is examined--it would make sense to assume that an equal percentage of radiation patients would actually be at a higher gleason level than their biopsies show.

Blackjack, I've seen it quoted that it's about 30% total change, and about half and half. Regardless, if there are that many upgrades after surgery, it makes sense to assume that there are an equal number of "upgrades" for radiation patients.

This is a sad tale but does not surprise me at all. Research conducted looking at over 100 genetic markers accross the Gleason 3 and 4 patterns concluded that PCa risk cannot be stratified by Gleason. Gleason is nothing more than an approximation (architectural) interpretation of PCa cell structures. The study identified 5 marker clusters based on dna copy rate/replication failures as a more precise means of determining aggression and progression. You will even find members clinging onto % of G3 and G4 and G5 differentiation in biopsies and pathology reports trying to stratify risk. We are I am afraid in the dark. Those that have long survival or often do well post post RALP are nothing more than the beneficiaries of less aggressive disease. G3 can be as lethal as G5 and we have many cases of G5 living for 15+ years . Bottom line. It’s a crap shoot. Sorry for the reality check.
Fresh

Bottom line: a biopsy, even a fusion biopsy, is not the definitive word on an individual's case. Maybe the future will bring improvements in gene markers and better definition (let's hope). For now, coasting along with a low risk diagnosis is not as risk free as it sounds.

GFB: So sorry to hear a "Brachy Brother" with recurrence as this is quite rare on this forum. What is your next step? Sounds like the spread is regional and can be hit with the aide of a good RO's advice. I greatly appreciate your imaging diligence as this is excellent advice for so many others on this forum. Please keep us informed as our thoughts and prayers go with you.

Fresh said...
This is a sad tale but does not surprise me at all. Research conducted looking at over 100 genetic markers accross the Gleason 3 and 4 patterns concluded that PCa risk cannot be stratified by Gleason. Gleason is nothing more than an approximation (architectural) interpretation of PCa cell structures. The study identified 5 marker clusters based on dna copy rate/replication failures as a more precise means of determining aggression and progression. You will even find members clinging onto % of G3 and G4 and G5 differentiation in biopsies and pathology reports trying to stratify risk. We are I am afraid in the dark. Those that have long survival or often do well post post RALP are nothing more than the beneficiaries of less aggressive disease. G3 can be as lethal as G5 and we have many cases of G5 living for 15+ years . Bottom line. It’s a crap shoot. Sorry for the reality check.
Fresh

I’m not so sure if we can throw out Gleason risk classification out. It’s logical and scientific and is somewhat correlated with genetic abnormalities to the extent we currently know. If a cell is well differentiated (g5, g4) , it’s mutated enough from the original cells to have a different cell structure. Very seldom you see G6 from a post RALP with negative margins and with other low risk classification ( LN-, SV-, ) going to BCR and metastatic PCa. Point being Gleason score matter. What we don’t know is if during primary treatment some cells survived and that’s all it takes - there is an element of luck, some may call it the unknown. Good news is If we all survive next 10 years which I hope we all do, we may have better option than HT.