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Whadda you think?? Do gleasons migrate higher.

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Posted 7/20/2010 8:46 PM (GMT 0)
I think they do, but have no real documentation, just my own case. I believe there are cases where it will start with 8,9 or 10, but also believe 6 and soft 7's 3+4 will over time also get more aggresive. It just makes sense to me. And as Judge Judy says if it doesn't make sense it probably ain't true.
Posted 7/20/2010 9:06 PM (GMT 0)
According to my Radiation Oncologist, that is generally true. Type 3 cells can mutate to type 4, type 4's can mutate to type 5. These further mutations would increase the Gleason score. The trick though, is that there is such a variation in how long these mutations take place. For many men, they never mutate in their normal life time, and they will die of some other non-PC cause. Any Gleason with a "4" in the mix is risky, as "4" cells are very unpredictable. Sometimes they act more like "3" cells and aren't aggressive, and sometimes they can act like "5" and be very aggressive. The difference between a Gleason 7 3+4 and a Gleason 7 4+3 is more than it looks on the surface. To my surgeon, and many surgeons, they don't view them greatly different, because they are going to be removing the prostate anyway. To the radiation oncologists I have spoken with, it can make a big difference, due to the greater number of "4" cells in the mix. No Gleason 7 should be taken lightly in my opinion, its not at all like a verified Gleason 6 case This is some current thinking, where some doctors want to treat Gleason 7 cases as if they were Gleason 8 cases.
Posted 7/20/2010 9:08 PM (GMT 0)
They absolutely can. Either by time or detection.

Gleason sums are a combination of two Gleason scores. Take mine for example 4+3=7. One could say I am a Gleason 8 with lass tumor. (same for a 3+4 guy). It's not the Gleason sum that will be your problem if things take a turn for the worse. It will be the highest grade detected at that point. I feasibly can have the same amount of G3 cells as today, but if those G4 cells grow uncontrollably, my disease characteristic will be more of a Gleason 8. What's more, your Gleason sum is a combination of the two highest grade cells detected(or a third in a case where a tertiary score is provided). It's always possible that there are higher grade cells that were not detected...

Tony
Posted 7/20/2010 10:54 PM (GMT 0)
From what I have read there are agressive cancers and non agressive. Non agressive PC will not progress. The evidence is that 70% of G6 pc never progress and that even when there is extra capsular extension with a G6 it rarely mastastizes. Unless it is a varient no one dies from a G6 PC.
There just isn't a normal progression from G6 to G7 to G8 to G9. There are too many instances where the initial diagonosis is G8 or G9 without going though a G6 or a G7.
Most certaintly there are some G6s that given enough years will get to a 7 or an 8, but most will remain G6. There are a number of varients that act totaly different from normal PC cells and these are what will mutate rapidily; about 2% of G6 PC are varients.
JT
Posted 7/20/2010 11:11 PM (GMT 0)
I think that the best evidence that most PC never progresses is that 50% of all men at 50 years of age have some sort of PC and it rises to 60% at 60years old ect. Yet only 16% are ever diagonosed with PC and only 2% ever die from it. If most PC progressed to G8 or G9 a very high proportion of 50 year olds would be dead in 30 years, especially those that are undiagnosed, and this is just not happining.
JT
Posted 7/21/2010 12:49 AM (GMT 0)
But...

1. For men that have a biopsey, not surgery, there might be higher grade cells that are not sampled.  This isn't progression, but it means that if the biopsey is 6, it could be upgraded to a higher number with surgery.

2. To say that a Gleason 6 never progresses to higher grades, that means that someone has followed a group of patients for the rest of their lives with biopsies and never saw a higher grade show up.  Do you know of a study like that?  If some one has done a study with no progression at 2 or 3 years, it could just mean that it takes a longer time for the progression to show up and be detected.  The trouble with most of the studies of prostate cancer, like the studies that are supposed to show little benefit from PSA screening is that the studies look at patients for a few years, but the disease unfolds over decades.

3. For people that have Gleason 7, 8 or 9, where did that come from?  Were they high grade from the moment the first cancer cell occurred, or were they Gleason 6 for a while till the higher grade developed?  The fact that low grade and higher grade cells are typically found together on biopsies suggests that the latter is the case.

Posted 7/21/2010 1:26 AM (GMT 0)
I wonder what the expert pathologists have to say on this issue. They are the ones that find them on biopsy or post-op pathology. For my case was the tertiary foci of 5 found in the midst of 3 or 4 or out there in the boondocks. For that matter when you have a 3+4 are they isolated from each other or all kine mix up. Somebody in the field knows the answer to these questions, maybe some day they will tell us. The reality is as TC said its the highest in the mix that will ultimately do the damage over time. God bless us everyone!!
Posted 7/21/2010 2:38 AM (GMT 0)
My opinions don't mean a lot on these tyoe of topics. It would be unusual in my opinion for a cancer cell which is already a mutation, to continually mutate to a different type of cell. Would never say they don't or can't.

In my case, I have had yearly PSA's since I was 45. Low PSA, no sign of issues until I was 57. My first biopsy because of a lump on my prostate showed no PC, just some high grade PINS.

One year later, a biopsy showed Gleason 9. I can only assume that those cancer cells started out as Gleason 9's.

I think John's comments are right on the money on this subject.
Posted 7/21/2010 4:23 AM (GMT 0)
I found part of an answer to this question:
Prognostic Markers Under Watchful Waiting and Radical Prostatectomy
Holmberg et al Hematol Oncol Clin N Am 20 (2006) 845–855

Patients randomized between watchful waiting and surgery.

Gleason <7 at diagnosis, waiting group: 8% risk of death from prostate cancer in 10 years, surgery: 4% risk
Gleason <7 at diagnosis, chance of ever receiving hormonal treatment after 10 years: waiting group, 52%; surgical group: 23%

So, more than 90% of people with Gleason 6 are alive at 10 years, even without treatment at the time of diagnosis, but it's not always benign. Also, the graph in this article (Figure 5) shows the hormone treatment graph is 52% and is still climbing quickly at 10 years in the watchful waiting group, so something's causing those people to take hormones. Maybe some Gleason 6 is benign and never makes trouble, but another possibility is that it just gets worse very slowly. If you have a few microscopic prostate cancer cells like most older men, it won't catch up with you till you're 120 years old. If you have a lump of it that's big enough to stick with a biopsy needle, and you live 25 years, maybe it could make trouble, who knows until someone does a study with a 25 year followup.
Posted 7/21/2010 10:24 AM (GMT 0)
Maybe we are all born with a few microscopic PCa cells and they multiplied as we got older ... and then maybe some of us just were better at cultivating the little devils then others (i.e. diet, environment, lack of vitamin d, agent orange, etc.).
Posted 7/21/2010 12:48 PM (GMT 0)
The ploidy analysis (the DNA structures have been found to change over time and advance ones PCa aggressiveness...what triggers it...probably at the cellular level PCa receptors (many different ones like one is p53, another variable is called pTen and there are many more), once changed can break the DNA link and end up with other than diploid (two indentical pairs of DNA strands, which is our normal cell structure pattern). Diploid status is where early PCa is usually found most commonly, anyway (67% from pathology on Gleason 6's from a large sampling). It might change overtime and become aneuploid which is not the normal set pairs of chromosomes we are found with originally, becomes more random or chaotic in structure. The aggressive cancers are usually found with ploidy of aneuploid or used to be another level (maybe still is) called teteraploid (super chaotic). I guess this is part of the gig, also helps explain how PCa morphs and becomes resistant to certain drugs after awhile. Simplistic???? The DNA can change, so in effect the cell is now different than the original...when that happens???? (varies) Not to mention 18 variant types of PCa identified (or more) by the expert pathologist guys.
Posted 7/21/2010 1:52 PM (GMT 0)
If Pca can mutate to be more aggressive, that would indicate another reason to have treatment when Pca is first detected and forgo the option of active monitoring.

Since pca can mutate to become more aggressive, can it also mutate backwards to become less aggressive? My dad was a gleason 8/9, so does that mean a higher chance of being diagnosed with a aggressive pca then someone who has no family history of it?
Posted 7/21/2010 2:08 PM (GMT 0)
I asked my uro that question when my biopsy was Gleason 8. His response was that it was not always Gleason 8, but had progressed to that point. This did not thrill me, as 12 months earlier another uro had assured me I only had BPH and chose not to do a biopsy.
Posted 7/21/2010 2:16 PM (GMT 0)
Squirm:

No, there is no way a cell is going to mutate to a lesser agressiveness. Wished it worked that way, but not going to happen.
Posted 7/21/2010 3:26 PM (GMT 0)
Found one article about PTEN (gene)this is the gene discovered in 1997, in prostate cancer Pten loss has been associated with progression to androgen independence , chemoresistance, radioresistance, bone mets and disease recurrence after surgery. Pten loss significantly correlates with higher Gleason score, poorer prognosis and higher serum PSA levels, although Pten loss cannot predict prognosis. (interesting?)

Pten is found on chromosome #10 (located on the long arm of chormosome 10 at position 23.3)- whatever that relates to! So, they have identified it and know some of its features is the good news.

Source: BJUI International (Journal Compilation 2009 104, 556-561)

I guess this is: BRITISH JOURNAL OF UROLOGY, INTERNATIONAL
Hey I got it from my onco-doc, it looks like an International Journal Publication thing.
Drs. Chris. Uzoh, Claire Perks, Amit Bahl, Jeff Holly, Marto Sugiono and Raj Persad: all from the U.K. (published Nov. 14th, 2008) (full reading would be a great idea for anybody)

Pten= Phosphatase and TENsin homologue deleted on chromosome #10 (thus the name)
Finding out the how and why the chromosome got deleted is key in PCa and this article talks about that in details I cannot relate to, if you thought you were good in biology read it and see if you can comprehend it to put into synopsis for laypersons. I am just pointing it out and can get the concept that chromosome changes effect PCa progression or risks.

Twilight zone is easier to comprehend! yeah

Post Edited (zufus) : 7/21/2010 9:51:08 AM (GMT-6)

Posted 7/21/2010 4:12 PM (GMT 0)
Interesting thread....so correct this thought pattern for me.

If the DNA is altered by our gene's heredity (born with bad genes) then it could be possible to determine through testing who is suspect and in what degree or gleason could be expected down the road. Reason I know this possibility was due to DNA testing for Alpha-1 which I have. But the caveat is that if the DNA mutation was caused by environment (diet, chemical exposure, radiation etc), then there is no way to determine what cancer will develop, where and to what degree.

I think I remember that radiation attacks the DNA in the cells, thereby destroying the cells ability to mutate further or replicate. And if radiation mutates the DNA, then there is always that chance of creating cancer like mutations in healthy cells.

Is my thinking flawed?
Posted 7/21/2010 6:45 PM (GMT 0)
Les,
From what I understand a normal cell is damaged some how, by chemicals, constant inflamation or just inherited genes. Most of these cells never grow and just die; a few may rapidly reproduce and this is cancer. There are certain things that fuel the growth, testestorone, sugars, animal fat and protien are thought to be some of the things that fuel cell growth. Cancer cells are much more effected by radiation than healthy cells. Cancer cells will not be able to reproduce after radiation, while healthy cells can usually repair themselves after radiation exposure.
JT
Posted 7/21/2010 8:39 PM (GMT 0)
LV-TX (I don't profess to know the answers), good questions it seems your first one is yes to some degree, once they figure out the DNA and genes they can gleen somethings, like breast cancer has hereditary mutations in BRCA1 or BRCA2 genes identified that causes breast cancer. So likely yes to your first question is they should be able to determine these suspect genes and inhibitors that work with them. The P53 PCa gene is very envolved in our disease. I don't know if it could relate to knowing a Gleason score for PCa, idea from such information (??).

Like John T said on radiations, this is what is known and mentioned about how it works. There is a risk factor on radiations (probably todays radiations risk factors not even comparable to 20+ yrs. ago or more for collateral damages). Considered safe, but also there is possible cancers that could happen from radiations, I guess the CT and bone scans and such (considered safe) but could have a risk factor and multiple exposures to radiations could increase those risk factors. I have no idea what level those risks actually could be(presumed low), maybe some one has seen an abstract or information on that.
Posted 7/21/2010 9:29 PM (GMT 0)
Thanks JohnT and Zufus

While there isn't any prostate cancer history in the family (except me), there sure is a boat load of other types of cancers along both genders. So doubtful in my case heredity being the cause, but all the other things environmental...well what can I say...the 60's were really good.

I guess I am like most folks...would like to know why I got cancer and what caused it.
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