This article by Dr. Dan Sperling is kind of discouraging for guys like me with Extracapsular Extension, especially the last paragraph:
“Compared with organ-confined disease, prostate cancer with extracapsular extension is associated with decreased overall and cancer-specific survival following radical prostatectomy.” Patients found to have ECE are typically be sent for a course of beam radiation and/or be put on androgen deprivation therapy as a management strategy though it is not curative."
ECE (Stage T3a) is a high risk factor, as is psa>20 or Gleason score of 8-10. High risk has inferior outcomes to intermediate or low risk. Still, outcomes are very good.
In the ASCENDE-RT trial, high risk men getting brachy boost therapy enjoyed 9 year biochemical recurrence-free survival of 83%:
pcnrv.blogspot.com/2017/03/...
At top institutions offering this therapy, high risk men had 10-year cancer-specific survival of 87%:
pcnrv.blogspot.com/2018/03/...
5_plus_4 had a RP and I believe adjuvant radiotherapy.
How does this treatment compares with RT plus brachy boost? The Kishan study is not a RCT, it is a retrospective study , and they compared RP but they did not compared RP plus adjuvant RT.
It was not an RCT - but it is the best quality comparative info we have. Kishan looked at those who had adjuvant RT after RP and found mortality was twice as high with surgery+EBRT:
pcnrv.blogspot.com/2018/11/...
I think you'll agree that until there is an RCT (which will probably never happen to today's standards), this is the best info we have.
In the first Kishan study you mentioned there were only 3 cohorts:
"Patients were grouped into 3 cohorts based on the definitive
local treatment received: EBRT, EBRT+BT, or radical prostatectomy. )".
I could not find a comparison of RP+adjuvant RT vs EBRT or EBRT+BT.
sci-hub.tw/https://jamanetw...
The response of Kishan to a comment to his paper (included in your last reference), shows the comparison with of EBRT+BT vs RP+EBRT and there was a survival advantage for EBRT+BT.
However, Kishan said:
"The
results are consistent with the previously reported outcomes comparing the overall radical prostatectomy cohort vs the EBRT+BT cohort. We acknowledge that these subset analyses are likely to reflect selection biases, which is why we did not previously report them.:
Kishan himself doubts the value of the results reported when answering the comments to his paper.
The comments to Kishan's paper done by Ong illustrates some of the problems with the Kishan's paper:
"Second, patients with Gleason scores of 9 to 10 are
at high risk of micrometastases at the time of radical treatment. Biologically, it seems unlikely that local control with
radical prostatectomy is sufficiently inferior to EBRT+BT to
explain the observed differences in outcomes. However, more than 90% of patients treated with EBRT+BT had androgen deprivation therapy, whereas among men who had radical prostatectomy, 19% had some form of neoadjuvant androgen deprivation therapy and another 10% had adjuvant androgen deprivation therapy. The observed benefits of EBRT+BT over radical prostatectomy could be confounded by the effect of androgen deprivation therapy given to a higher proportion of patients with EBRT+BT. "
sci-hub.tw/https://jamanetw...
The Tiki's paper is not a RCT .
sci-hub.tw/https://jamanetw...
None of these is an RCT, and there will probably never be an RCT with proper comparisons. Until then, we have to make judgments based on the best information we have. The multi-institutional Kishan study, at some of the top institutions in the world, and using propensity score matching, is our best source of data. I just showed you a comparison of RP+adjuvant RT vs brachy boost, so I don't understand why you can't find it - click on the link and a comparison chart will appear.
Far from doubting the findings, he believes the superior result of brachy boost may be attributable to the long use of adjuvant ADT used with it. I'm told that a forthcoming Australian study seems to bear out his hypothesis (an update of the TROG 03.04 RADAR RCT) .
I think all high risk men should receive an advanced PET scan to rule out distant micrometastases before any kind of radical therapy is used.
He said what I quoted from the paper, "We acknowledge that these subset analyses are likely to reflect selection biases, which is why we did not previously report them."
it is powerful to me when a researcher decides not to report something in the original paper, They thought the lower incidence of ADT treatment in the RP group when compared with the EBRT +BT may explain the differences in outcomes, but they do not know for sure,since this was not a RCT.
You said : "Far from doubting the findings, he believes the superior result of brachy boost may be attributable to the long use of adjuvant ADT used with it".
I believe you are saying that the method of treatment is not responsible for the difference in outcome. The better survival in EBRT+BT is due to a higher incidence of adjuvant ADT treatment in the EBRT+BT when compared with the RP+EBRT. But again we do not know for sure since this was not a RCT.
I agree high risk PC patients should receive advanced PET CT scans to rule out distant metastases and to guide local therapy if necessary and possible, This was discussed by Dr. Fanti at the recent APCCC 2019 meeting:
urotoday.com/conference-hig...
There is limited space in a journal publication. There is always data that is left out. Kishan will publish future articles based on this data set. Subsets are always problematic as the sample sizes are diminished. Even so, his sample size was 436 treated with BBT vs 80 in the Tiki sample; for RP+EBRT, it was 272 vs 128; and for RP+ADT, it was 175 vs 99. Whichever way you cut it, the Kishan sample is bigger than the Tiki sample, and is more reliable (given similar methodologies).
I wish we had RCTs to rely upon for each decision we make, and that there were adequate subset analyses to cover everyone's case. Unfortunately, as I said, we will never have that. Therefore, we have to analyze each study carefully and draw conclusions based on the weight of the evidence. Kishan's study remains our most reliable, and probably will for a long time.
Longterm adjuvant ADT is part of the BBT treatment as given at those top institutions. When RP is given with adjuvant ADT, the the adjuvant ADT was shorter (except when positive lymph nodes were discovered). So I agree with Kishan that the method of treatment is responsible for the difference in outcome.
I would also add that adjuvant RT after surgery has especially high rates of permanent incontinence. If someone is going to have radiation anyway, it is best not to have it after surgery.
Remember that there is a built-in bias towards survival with surgery, because men are 5-10 years younger, and men are allowed to go through radiation who are otherwise too infirm to go through surgery. Unlike database studies, there was more data available for matched cases, although there are certainly variables which could not be captured. Selection bias favors surgery. Even with that bias, brachy boost therapy has about twice as high prostate cancer specific survival in matched cases.
Amen
Amen to the pet scan prior to any treatment. If it can find cancer in early stages why not use it for yearly checkups. Should be as easily accessible as an X-ray. It’s a scan not a drug. FDA needs to get of their high horse and find a way to get them in every hospital. The only people that die are the guys that have drs that don’t do exams or urologists that miss on biopsy. Look around at the cost to treat this when it’s to late and tell me we can’t have 10,000 scans around this country. I’m talking about the USA.
"Amen to the pet scan prior to any treatment. If it can find cancer in early stages why not use it for yearly checkups. "
PSA tests are good enough to let you know if things are stable or are growing.
If the PSA test shows something is growing again, then you use the pet scan. Less cost. Less Radiation.
I’m talking about yearly visit to your doctor. We all get X-rays every year. How many of the guys here would have had surgery one and done if the test was good enough to say it’s positive at a very small size. We get a finger and a biopsy that misses when it’s curable. Stupid if the test exists.
"We all get X-rays every year. "
I don't. They just keep an eye on PSA unless and until they see something rising. Should I be getting scans on a regular basis?
"We get a finger and a biopsy that misses when it’s curable. Stupid if the test exists."
I don't understand. Can you say that in different words?
I would like to see the very best pet scans used as first test for year.y check ups starting at 50 years of age.
In my case psa did not catch it early, neither magnitude nor velocity. Dr said 5% of men like me, true or not who knows. So still looking for confident indicator post treatment. And still working on collecting info to better refine risk estimate to decide on best treatment for me. 3,4,7 gl. Pni. 2nd opinion on biopsy coming. Wondering which genome test is best, like they are not consistent always. Wondering if pet scan helps. Interested in perspectives, thanks, 45.
Guys, you lost me at RCT. Whatisit? In fact, a few less abbreviations might us, the uneducated, keep up.
There is a nice list of acronyms on the advanced prostate cancer forum main page. Helps to avoid confusion--- Random Controlled Trial
"I did not know that"
Johnny Carson
Thanks, I'll look up what I don't know.
Agreed. I try always to spell out words here. I personally think it's very very ill mannered to toss around these cryptic acronyms in a forum meant to help others, many of whom have just been diagnosed.
I agree!!!! The unfamiliar acronyms are very confusing and cause some, like me, to not understand what's being said. I know some on this site are very well informed but others need a bit of help. Usually when you use and acronym you give a definition the first time it's used...surely this wouldn't be too time consuming ... it's too confusing to keep going back to main pages for the definitions as you can lose the thread of the argument or line of thinking.
I'm getting better at it. But I think our regular expert posters could use the standard style you refer to:
Spell it out the first time you use it, then follow with the abbreviations.
It would be courteous.
Meantime, I will keep bouncing back to the top page list.
There is just so much important information here not to go to the extra trouble to be able to understand as much as possible.
Yep I agree...lots of invaluable information.
I was T3a (ECE), Gleason 8, 15 years ago and today I am still asymptomatic. Only adjuvant therapy was the removal of a few LN's.
I’m t4 gleesson 8 hoping for your outcome
Well Carlo ,I too had the same scores . T4 sucks .. ronron is the man . Good luck ✌️
As Tall Allen mentions, ECE means a high risk factor; translated means shorter life span. In 2009, age 62, very fit and mainly super healthy, I was ECE, and inoperable, Gleason 9, 9/9 positive biopsy samples. Trouble was that Psa was only 6. I'd organised the uro surgeon to give the biopsy, because system says to act when Psa reaches 5.0, which I did, after years of yearly tests. I was in the 1% of cases where surgeon could not continue with RP after opening me up.
So I began ADT, and 6 mths later had 70Grey EBRT when PG had been shrunk down to small target for RT. Psa has been up / down like a yo-yo for many treatments, but 10 years later I have survived. Psa never has exceeded 50, and is 0.4 now, after recent LU177 treatment.
ECE often means there is so much Pca outside capsule and adhering to outside of capsule that docs cannot safely remove the outside Pca without cutting many nerves, and also causing probable mets spreading to many places. But I have met many men who had RP and Psa went low, but rose fast a year or two later because a small amount of Prostate tissue was not removed, and it may not have had Pca at time of RP, but later it develops Pca like the first early Pca cells.
My surgeons decision to not do the RP and refer me on to ADT + radiation meant I had a pretty good QOL and I have always been fully continent.
I maintained a high level of fitness with ADT that did not decline compared to many other men I have known of same age with a full bottle of testosterone.
It does not matter that my treatment has exterminated all my sexuality because I was single before Dx, and I found 99% of single ladies at that time to be allergic to men, especially if they could cycle 100km easily. Not one woman has ever tried to understand my condition except the angelic nurses at the hospitals. Men are supposed to fully understand and care for women and all their problems, including their "pausing from men", but they often just can't understand let alone have any desire for man their age of older, especially if he has Pca.
If I'd had a biopsy in 2004 with Psa about 3, Pca probably would have been found and an RP might have been as effective as it could ever be with many men, none of whom post here because they don't have a problem after many years of Psa < 0.01, ie, undetectable.
One man I know had PG + bladder removed, ureters to Rodger cut off short as possible, and a stoma formed on side of lower abdomen, both ureters from kidneys taken to stoma, and he wore a plastic bag for rest of life like 50,000 other ppl in Australia where I live. The op cost a fortune, but he never had any Pca grow later with rising Psa. He kept his testosterone. He does not like to talk about this thing ever again. I have no idea if Viagra gave him a hardon and allowed a pleasurable climax. His marriage survived. He's had years of more good life, extended the house, travelled OS......
Brachytherapy+EBRT can often deliver enough RT to PG any Pca there to get rid of Pca, but a high Psa and Gleason at Dx means there is very high probability that Pca has spread away from PG, and scans may not see these mets for years, and from little things, big things grow.
The BT avoids the damage to rectum and bladder. But the total high BT+RT to PG and its Pca will often damage nerves all around PG that years later its the equal to having them all cut though causing ED and incontinence.
You need the best doctors you can afford.
Patrick Turner.
I'm struggling to apply this discussion to my own personal level. At diagnosis:
PSA 2.14
MRI: PIRAD 5 of 5
Extra capsular - seminal vesical
BIOPSY : GLEASON 8
METS : spine & tibia - later shown to be false positive
6 month Lupron - 29MAY19
Starting Radiation Treatment Monday September 23rd.
So, the earlier dx of PCa is now PC. Does the extra capsular growth make the diagnosis High Risk (for understanding the above discussion)?
Would it be reasonable to push for brachy-boost following the RT? and/or maintenance ADT?
Would it be reasonable to push for PSMA scan?
gps
My perspective, having been in a similar status in 20017 with ECE after RP, and also seminal vesicle invasion.
This calls for some form of salvage RT, whether that is EBRT or BBT that is chosen.
I would wait on the PSMA PET scan until after that is done and recovered (assuming PSA is still not-zero after the RT). Then it would be worth doing the scan to see where else it may be.
My understanding is that adding at least some short term ADT to the RT regimen improves the results.
ECE makes the cancer high risk. So does Gleason 8.
In brachy boost therapy, they reduce the external beam to about 25 sessions. You may be able to get an Axumin scan, but insurance may not authorize it.
Best to get PsMa Ga68 scans with Psa between 0.2 and 10, so it will tell you more where your mets are and state of PG.
AFIIK, you could have Lu177 if PSMa scan shows its worthwhile. But there are rules about who can get it, and its not yet fully approved in US, but its available for sale in Germany, India, South Africa, Australia, UK, but you need to get a doc to refer you, and have PsMa scan, and then confer with docs giving Lu177, probably using Skype. Cost is never cheap, but what is being alive worth?
Any Pca outside capsule is high risk because it is probable that Pca has already spread a lot, and that any PG operation is impossible without doing more harm than good. I I have my PG still, and it must be a real mess by now.
But I am still fully continent, and whatever tiny amount of Pca in existing PG is not a threat - its the mets that are the main threat, but they are at present under control.
I was in this ECE situation, Gleason 9, a real bad diagnosis. Psa was only 6.
But its now 10 years later at age 72, I am alive, and cycled about 30km OK, Psa 0.4.
Hello Patrick ..Removing the bladder was a brutal pill for your friend ..I’m sorry about that.. I read that and realize how fortunate I’ve been compared to so many of our brothers . I appreciate your honesty in posting . How is your fitness level now?
My friend did not want RP or ADT or EBRT or BT which have high failure rates and lots of side effects. So what else did his urologist have on offer?
The urol explained the bigger more drastic op, and my friend eagerly said YES PLEASE. There was no bitter pill, he knew getting old involved getting "various ills" and wanted surgery most likely to end the Pca problem, which it seemed to do. Wearing a bag for a Litre of urine was no problem. No waking up 5 times a night, no always looking for a toilet. Bag emptying is in seconds.
My Pca is under control, Psa 0.4, down from 25 before Lu177. Had 3 months of winter not cycling, and no hard exercise. Got back on bike 16 August, now can cycle 50km, a bit slower due to a hip problem that is not the cancer or arthritis in the right hip joint, but something to do with a tendon connected to femur and tear in right gluteus max muscle, nobody knows exactly what despite MRI.
The hip soreness why might be due to previous RT to sore area = 17Grey from EBRT to PG path way in 2010, plus 7Grey from additional IMRT 2016, plus 20Grey EBRT to hip last June, so 44Grey total. Its enough to maybe cause permanent damage to healthy tissue. It its not enough to cause much discomfort with low exercise living but was likely to happen by attempting to spent an hour+ a day doing serious exercise. But I should soon work back up to cycling 30km easy across town to very good coffee at the Little Istanbul at Tuggeranong - and then cycle 30km home.
Massaging soreness in muscle is making it slightly better.
Weight has declined 2Kg since July, "peak fat" time for me and is below 84Kg for first time since Feb, despite taking enzalutamide that is supposed to cause fatigue and weight gain. Not in me it don't.
BMI < 25, waist < 95cm, resting HR > 50, all blood test items OK. I am not doing too bad for an Old Bar Stud.
Stay well Lulu700,
Patrick Turner.
I’m happy to hear that you’re back to biking . You are inspiring ..I had a bit of the tubes out of my kidney for a year .. I felt for you friends plight . True ,we do what we must . We ‘ve moved up hill in Arizona 200 miles to a bit cooler climate . Life is good right now . We live with gratitude.. Tuggeranong ,great names you have down there.. To know that you are biking to and fro cheers me up mucho . Luckily I’m not gaining weight either ,but I do have fatigue in general . “ all blood test OK .. that’s positive .. Thanks for posting ..Keep rolling Patrick -T 🚴♂️
About all I can add to this discussion is that doing a biopsy at PSA=3 or PSA=4 (the standard of care in many countries) has failed a few of us. I was ECE from day 1. We absolutely need more tools to confirm PCa before it becomes ECE. I am not seeing any research published in this space.
I could not agree more, but Dx at Psa 3.0 would prevent many men having expensive long battles with Pca.
If you were ECE at Psa 3, at Dx, then any following ADT+EBRT or ADT+BT would probably give you are better outcome than if you'd been diagnosed when Psa was 6, maybe years later, when the Pca might have spread locally plus to distant mets. Regardless of ECE or not, early Dx with low Psa probably gives a longer OS survival time and maybe a lot less expense on following treatments.
When I was diagnosed, scans could not see Pca in PG very well. Now the MRI can show more.
A few years ago another chat group on Pca existed. It was administered by a man with Pca who got so sick with it he could not run the group so it became full of viruses and didn't function. But before that happened there were men there who said they had biopsies when Psa was only 2, and they repeated this each year, and then BINGO, 3rd biopsy at Psa 3 found Pca, and they did not dither about with "watchful waiting" but had the PG removed, thus ending their Pca threat immediately, forever. Many men hate going to a doctor. Some go so regularly. They paid more than most, with a biopsy cost over $1,000. But total expense later was low. Some have strong family history suggesting they would be a fool not to get examined and treated way before most other men.
Patrick Turner.
Patrick, thanks for the extensive report.
Yesterday was my first RT day.
Close parking? Validate parking? Street clothes? Sweats? Trying to learn everybody's names.
From you guys, I'm learning that just because I don't have verifiable METS, it's probably not going to be just zap x 40 and forget it ever happened.
You won’t forget it . But it possibly can knock out the pc . I did 8wks x 5 per week . That along with adt kept me clear so far over four years. Good luck and heal yourself ..
👍
I began ADT in April 2010. 8 months later in Dec I had 70Gy EBRT in 35 daily shots. The ADT before RT shrunk the size of ADT to make it a smaller target thus minimize damage to bowels.
Psa went from 8.8 to less than 2 at RT. Then ADT continued with Eligard for 16 more months.
Then I quit having the Eligard shots in late 2012, to see if the treatment I had worked. Psa nadir had been 0.08, but soon Psa soon zoomed up to 8.0 within 6 months, and at no time did I assume I was cured.
But in that time, testosterone came back, I was able to cycle 4kph faster average speed, rejoin "fast group" I used to cycle with, no more ED, and it was like being reborn.
I went straight back to ADT in about May 2013, and soon lost 4kph average bike speed, joined a slow group to ride with. Psa went to 0.2 nadir, then slowly began rising and it became rapid rise in 2016.
Cosadex was added to ADT. Then I had 31Gy salvation IMRT to PG, but reduction of Psa was brief, and I doubt the IMRT or EBRT did very much; ADT seemed to do most to keep Psa low. Next Psa Nadir was 0.4. Not as low as before.
It seemed I had Pca that was radiation resistant, not uncommon. I met men who had the same amount of treatment I had and they got remission, but their Gleason at beginning was low, Psa about 5, so they had Pca that was a weak, a pushover wuss.
The EBRT to PG was easy to tolerate, and I cycled over to hospital each day for first 2 weeks, a 35km round trip. Then I got a burning sensation when I peed, so I stopped cycling. Burning pain continued until 2 weeks after EBRT finished, then back on bike, and life continued. It was agony to pee, but not something I could not handle, and no painkillers helped, so just grin and bear it.
There were usually 15 ppl in the waiting room for RT using one of several big RT gadgets. Most were completely silent, and did not respond to "G'day mate, how are you going?" It seemed they were in zombie mode, depressed, terrified, and truth be known maybe many had been told they'd be dying soon. There was a lady about 45, the youngest I saw there, who could not figure out why I was so healthy. She spoke a little, but the other ladies were very quiet. One man spoke more than the rest, and he said he was working in a palliative care centre, and Pca had come to visit him like the ppl in his care. We got on fine, but I didn't see him every day, and mostly it was just impossible to cheer up anybody, they all were deeply gloomy, except me.
I knew my treatment might fail, and I could die soon, but so what? I would not be worried after I did die. I was still working, could cycle OK, so why the gloom? But I did stop accepting big work contracts in 2009 after diagnosis, thus giving myself more time of my own.
Long term side effects of the 3 lots of RT I have had to PG and to a right hip have been minimal, and I am fully continent, but when I need to pass solids, I can't delay that for long. Other men may find incontinence and bowel urgency is chronic, they must live with a bathroom 3 metres away at all times.
I did think hip had radiation side effects to muscles so I worked out what total RT has passed through sore muscles near hip, only 17Gy. Muscles can take 60Gy to 80Gy without muscle fibrosis which makes them weaker, and sore for a long time if not forever. But my hip pain began before last lot of hip RT and so RT is not to blame, and after resting all winter I restarted cycling and orthopedic surgeon said I should keep going. So its possible healing though use is possible plus some massage. There's little pain when I ride and little at night, but a part of gluteous max feels sore, something is not right.
I did get a faith healing from a very nice 40yo lady who said prayers to ask God to heal my hip, but it seems no miracle followed, and that was 8 weeks back, plenty of time for any god to get to work and fix a bother. I realise of course that most gods have a billion or two requests each day, and might think there are others who have vastly bigger need than I do, so they might ignore this nice lady's request for a fix. OK, I forgive them for what they will not do. I'll just muddle on in my little old life without bothering any god.
Nice spring day here. Cycled a good 40km yesterday. I must travel to Sydney by train tomorrow for a nephew's wedding. I'm feeling well, and will enjoy the 3 next days.
Patrick,
Let me tell you how I see your story.
I see a warrior. One that's willing to face every new battle and give it everything. I see success.
When I began to comprehend my diagnosis my first plan was to have no treatment.
Hey, I bought a new phone on their 2 year lease plan. I told my daughter that I would probably die within a year, so I would have a great new toy for half price.
Then I started to read stories about heroes like Patrick who are at 9 years and counting. The 'never give up brigade.' You guys made me ashamed that I was considering giving up as a first option. You recruited me into your brigade. I'll take whatever treatment seems right and I'll put up with the side effects because that is what Patrick and the other heroes of this forum do.
I salute you and thank you for the time served. I'll do my best to live up to your (and all you other heroes) example.
My dear Granpa,
I need Lady Luck on my side but have Auntie Destiny sitting on one shoulder and Unkle Fate on the other, and I hear them arguing about how they'll use arthritis or cancer to kill me. I did invite Aunty Lutetia to invite herself to Pca parties going on all around me body, and it seems like she shot 'em up good with her alpha particle guns she kept tucked into her bra. Dat one good wild sheila fo' sure.
But getting rid of all Pca is harder than fighting Isis. Pca is trying to re-group I bet. I'll see who I can get to fight for me later.
Cancer patients need luck because not all treatments work, and I've seen men more determined than me go down fast.
Life's good, no? I reckon its great.
So, a nephew is marrying on Friday, I will be away next 3 days, I'm well enough to enjoy the wedding. Dat something,
Patrick Turner.
It’s just an article and not every body is the same. fight, live my mom had 3 horrible diseases that would have killed her according to every doctor but she had the will to live and she did
No surprise to me as a Gleason 9 pt3b PCa survivor! Still going strong at six years.
I had extra-capsular extension with no extension into the seminal vesicles (Stage IIIa), no positive lymph nodes or evidence of other metastasis by Bone Scan or Axumin Pet Scan (I tried to get a PSMA but my PSA was too low).
Gleason score was 85% Gleason 6 (3+3) & 15% Gleason 7 (3+4).
PSA was 9.7 before radical prostatectomy, 0.09 one month post-prostatectomy & 0.02 two months post prostatectomy.
Radiation treatment was started just before 3 months post-prostatectomy. I am completing a course of radiation therapy for residual microscopic disease .... 39 treatments with 28 done & 11 to go. Doc's are calling it "curable".
It seems to me the article was emphasizing the importance of the newer MRI methods & not so much a discussion of prognosis. The last sentence you refer to may be stating that ADT (Androgen Deprivation Therapy), (JUST ADT) is not curative ..... no news there.
The last paragraph of the article states .... "The pre-treatment information from mpMRI may be the determining factor, helping patients avoid the rigors of an aggressive surgical treatment when radiation may give them a better potential for cure." The last 4 words, better potential for cure, indicate to me PCa is curable with extra-capsular extension without distant metastasis. Distant metastasis (outside the pelvic region), indeed ANY metastasis, indicates a higher tumor load and makes a cure more difficult.
MUCH, helpful information by the many who chose to comment .... love all the study references .... THANK YOU ALL!!!! ALL of us is smarter than one of us!!!!
You do have to consider that ECE is only part of the story.
You can have an Gleason grade 7a or 7b that has extensions but after RP with the cancer left confined to the prostate bed and maybe the pelvic region, radiation may knock it out altogether or at least deal it a blow that will hold it for years, particularly if coupled with ADT.
A patient like this can go on for years before it spreads, depending on the exact profile of the tumour and the patient.
On the other hand you can have a Gleason 9 or 10 that looks capsule confined, post RP the PSA is zero but after months or even years it sticks it's paw up and waves from a group of distant metastases.
Not only the presence, but also the amount of ECE is a predictive factor. And also the surgeon skill means a huge difference for T3 patients. Surgeons should carefully assess the risk of ECE before surgery since its a delicate trade‐off between nerve preservation and absence of PSM. The best surgeons can fix both, the not so good fails with both. The difference between surgeons' results is (of course) never reported in the comparative studies between RP and RT/ADT as is the amount of ECE. I'm happy with my surgeon, T3a, 5 years and still undetectable PSA, good sexual function and fully continent.
All the posting here, deals with ECE with high Gleason score aggressive cancer. In 2011, I was diagnosed with low volume Gleason 3 + 3 prostate cancer and was treated with brachytherapy. I expected that to be the end of my cancer. Unfortunately, that was not the case to be. In 2016, another biopsy and an MRI found a large ECE about 1 inch diameter. I was treated with ADT and cyberknife. Now in 2019, I am under treatment with ADT plus Casodex for metastatic cancer in many lymph nodes.
Did not you already know of these stats prior to this article? I surely did .. we know what’s predicted for us . That doesn’t set us in cement to fall into the dismal ...
Any benefit to RP given likely extracapsular extension
A promising article. 
SRT with hormonal therapy, I need your help!
