A question

Jim, that's a good question to ask.

In my own case (just substitute my numbers for the example you used) is very similar. Had open RP, numbers started rising. Had Salvage Radiation, numbers started rising. Now, post surgery and radiation, have a fast rising PSA of 37 (April).

No, the surgery isn't allowing the cancer to spread. The cancer had already gotten loose prior to the surgery and/or radiation. PNI is one theory, as stray cancer cells can easily escape the prostate and prostate bed via blood vessels, which one doctor told me, are like a giant sewer pipe systems compared to the minute size of cancer cells.

In such cases, you can end up having clusters even, of cancer cells growing at mutiple sites aways from the prostate area, even before you have your primary treatment.

Hope this helps some on your question.

David in SC

brookp,

Hope HT helps , as my husband is responding well while starting it Feb. of 2012. We aren't quite certain if we are doing IHT vs. CADT.
What has your DR. recommended? Did he (she) put you on casodex prior to lupron shots?

Good Luck!

BOOGEE

I had RP 11 years ago - open not robotic and have had Zero ever since.

Not certain if it was the surgeon, the location (it wasn't out of capsule per Surgeon but pathologist disagreed) or just me.

My associate had RP and hasn't had a problem for 12 years with PSA

Maybe because we live right in OHIO!!!

Tom in West Central OHio

It has always been my belief that PCa is spread in high gleason tumors as a result of the biopsy. It seems to me that tearing out pieces of tissue with the resulting heavey bleeding could easily spread Pca cells locally. If they are of the hardy variety G8-10. They could easily take hold elsewhere.

More patients should be told flat out that any PCa treatment is still a gamble and no guarantees, even some low risk looking patients have failed to be cured, while some with little higher stats appear cured after 10-15 yrs. or such. So, the factors and I believe apparent reasons for this type of phenomena (all to common by the way) is: PCa cells can escape via PNI (perinureal invasion, they find a nerve/blood vessel source in the gland and can literally end up anywhere although lymphnodes close by are the first place usually to consider looking and sampling, some surgeons do not even sample nodes, some sample random numbers of them and it varies alot, so is this a best guess scenario , seem to have no particular rules so to speak).

You can have missed biopsies that have higher gleason scores or even another variant type of PCa, there are over 24 found types now known and even those can have different genetic molecular pathology i.e. the cause of your getting a PCa (many genetic ways). Now it is possible to be found with PNI in your biopsies and still perhaps be cured (seen in other patients histories), so that is a risk factor and not a black or white finding.We are dealing with plenty of non-definitives in PCa, alot of money on wasted scans, not enough patients likely being told the reality of this unreality....as it doesn't sell well to say we have a nice expensive gamble on this so sign up today and if that doesn't work their are more gambles and options that are further to choose from. I really dislike seeing statements like the doc says 'he got it all' (such b.s. he cannot see nor detect that he got it all...it is a blantant generality, better to say got it all in removing the gland itself and some docs have even botched doing that task). Be leary of any guarantees of no incontinence and other claims, many patients have heard such and found out it was not true, later and the hard way.

Dr. Barken came up with the terminology of micro mets, PCa cells in small quantities that can escape maybe via PNI or other possible ways and remain in your bones and such and not show up on any scanning methods today, but later on can multiple and account for a rising psa and maybe later on become visble upon scannings. This is apparently why someone could have 'curative' looking psa after surgery, but years later be found with PCa again, not really recurrence although stated that way, it was just dormant( see autophagy concepts) or micro mets that finally got enough production to be now detectable. That is my understanding on this, seems to make sense and accounts for what is seen in patients whom fail sometimes 5-10+ yrs. down the road. One thing we can see is it is an art and not simple science for treating long term incureable scenarios. (Dr. Lee and Dr. Myers examples of doctors whom have Pca and how they are fairing with incureable scenarios).

BB_Fan said...
It has always been my belief that PCa is spread in high gleason tumors as a result of the biopsy. It seems to me that tearing out pieces of tissue with the resulting heavey bleeding could easily spread Pca cells locally. If they are of the hardy variety G8-10. They could easily take hold elsewhere.

I think that that is an erroneous belief. The needle is essentially a hollow tube ------ it goes in and removes a plug from within the gland. Only tissue within the tube is removed and that tissue is one piece attached cell to cell by connective tissue. It's not as though the needle is dropping off bits and pieces as it is withdrawn. Likewise the bleeding. The bleeding occurs from severed minute blood vessels. Think of a clean cut ---- when you have a neat slice there are no bits and pieces dropping off the wound. Despite the claims of some docs who claim this of a biopsy (invariable they have a "less dangerous" test procedure to sell) there has not been one documented case of PCa being spread this way.
Bill