here's my 1am thoughts,
the growth rate of tumors. okay, 1st we know there is the gleason score
(a sum of the gleason ratings). 2nd the stage as expressed by T1, T2 and
so forth with additional letters and numbers to show where and how
advanced the cancer has spread. we also know that on average prostate
cancer is a slow growing cancer on average. cancer cells grow
exponentially, that is they grow by doubling each time they split. these
are the general facts.
so my 7 questions are: 1) can the actual amount of tumor be quantified
2) and these various growth rates plotted like a train schedule so you
can predict how fast it's growing? 3) and once it grows to a certain
size, plot the spread rate of it metastasizing? 4) there are partin
tables and other charts (?) but do these and other tables actually
answer these questions of time? 5) what effect are various well known
supplements on the occurrence of the tumor? 6) what kind of life
expectations beyond the five year mark are given for these predictions?
7) once the prostate organ is gone, does this mean the cancer cells will
grow at a different rate? remember once it does spread, they are still
known as prostate cancer cells; that is prostate cancer of the bone not
bone cancer. (there is something produced in the prostate that slows
cancer growth) hmm... things to ponder in the middle of the night, greg
Steve Kramer - 29 Dec 2003 11:07 GMT
1. You have no tumor nor are you likely to get one in the next few years.
The PCa that was in your prostate is now in a lab. If you had a tumor
anywhere else, they would not likely have operated on your prostate.
However, if and when you get a tumor somewhere else, assuming it is big
enough to be seen on any one of a number of scans available, it could be
quantified.
2. If you left a tumor alone, or maybe even non-mestatic PCa, you could
probably plot to a certain degree its growth, but then you'd have to take
into consideration the food you eat, your immune system, etc. If you treat
it, you can only observe the results.
3. See #2
4. No, they only show percentages of recurrence and cures.
5. See #2
6. It seems to me that anytime you have < 0.1 after RRP or LRP, the answer
is "we don't know". Once you have experienced recurrence and EBRT and you
are < 0.1, the answer is still "we don't know". If PSA goes up after the
prostate is removed and the bed radiated, I've heard "50% chance at 10
years," "about 8 years," and "7-9 years." However, that does not take into
consideration age, overall health, or even Gleason.
7. I don't know. My instincts tell me that PCa grows fastest while in the
prostate, but I could be totally wrong about that.
ADVICE: Quit pondering such things in the middle of the night. You only
lose sleep. If you lose sleep, your immune system doesn't work to it's
fullest.... Need I continue the rationale? The fact is, you could be
sitting there with no PCa left in your body. Or, you could be sitting there
with all your PCa sitting on your prostate bed just waiting for EBRT. Or,
you could have PCa swirling through your body and before it kills you,
science could come up with the cure -- or at least life-long suppression.

Signature
Wishing you a Happy New Year
Prostate Cancer Survivor (so far), not a doctor
PSA 16 10/17/2000 @ 46
Biopsy 11/01/2000 G7 (3+4), T2c
RRP 12/15/2000
PSA .1 .1 .1 .3 .4 .8
EBRT 05-07/2002 @ 47
PSA .3 .2 .2 .2 .3
Erection 05/12/2003 @ 48
Begin Lupron 07/21/2003 @ 48
PSA .1
> here's my 1am thoughts,
> the growth rate of tumors. okay, 1st we know there is the gleason score
[quoted text clipped - 18 lines]
> bone cancer. (there is something produced in the prostate that slows
> cancer growth) hmm... things to ponder in the middle of the night, greg
Leonard Evens - 29 Dec 2003 14:44 GMT
> here's my 1am thoughts,
> the growth rate of tumors. okay, 1st we know there is the gleason score
[quoted text clipped - 18 lines]
> bone cancer. (there is something produced in the prostate that slows
> cancer growth) hmm... things to ponder in the middle of the night, greg
There are studies which show on the average how fast prostate cancer
progresses depending on initial diagnosis. But there is still
considerable individual variation. The studies only tell you about
probabilities as they apply to a large group of men with a certain kind
of tumor. In some cases, the disease will progress rapidly. In other
cases, even for apparently aggressive cancers, the patient will never be
bothered by serious symptoms during his lifetime. As my doctor told
me, those are all statistics, but you are one person. For you, either
is progresses rapidly or it doesn't. You have nothing to lose by
assuming you will be lucky.
You should do everything you can to improve your odds, as long as it
isn't detrimental to your health. Unfortunately, nothing is known
conclusively about dietary factors which might help. Most of what is
known applies before you are clinically diagnosed with prostate cancer,
and it is not clear whether any of it applies after diagnosis. Some
things that might help slow the cancer down are (cooked) tomato
products, Selenium, Vitamin E, and Vitamin C. A low fat diet and
avoidance of trans fats and saturated fats may help. Losing weight if
you are overweight may help. Avoiding large amounts of calcium, the
equivalent of more than two glasses of milk, may help. (But if you are
being treated with hormones, you may need calcium supplements to avoid
osteoporosis, which would be a greater risk.)
Steve Kramer - 30 Dec 2003 15:41 GMT
> you are overweight may help. Avoiding large amounts of calcium, the
> equivalent of more than two glasses of milk, may help. (But if you are
> being treated with hormones, you may need calcium supplements to avoid
> osteoporosis, which would be a greater risk.)
I was in my uro's office this morning, and once again forgot to ask this
question.
I know that Calcium has been linked to PCa. I also know that Lupron may
play havoc with bone mass. Finally, I know that weight bearing exercises
and certain types of Calcium supplements (apparently some are absolutely
useless) will protect against bone mass loss.
So, what is the recommendation for a man on Lupron? Has anyone gotten an
opinion from their doc or legitimate medical sources?

Signature
Wishing you a Happy New Year
Prostate Cancer Survivor (so far), not a doctor
PSA 16 10/17/2000 @ 46
Biopsy 11/01/2000 G7 (3+4), T2c
RRP 12/15/2000
PSA .1 .1 .1 .3 .4 .8
EBRT 05-07/2002 @ 47
PSA .3 .2 .2 .2 .3
Erection 05/12/2003 @ 48
Begin Lupron 07/21/2003 @ 48
PSA .1
ron - 29 Dec 2003 16:24 GMT
Hi Greg...I'm not sure that definitive answers to your questions
exist, but here is some information / current thinking that may be
helpful...Best regards and good health, Ron
>1) can the actual amount of tumor be quantified
I assume you mean pre-treatment. Here is an excerpt explaining Dr.
Strum's tumor volume algorithm
From Dr. Strum about PSA leak and using it for volume of tumor. We
can use the formula of gland volume (GV) x 0.066 to give us what is
called the benign-related PSA value. If we subtract this from your
total PSA we get a result that is unexplained and we call "excess
PSA". This could be due to prostate cancer (PC) or due to
prostatitis. If PC, and assuming that the Gleason scoring is the most
common (3,3), we could approximate the cancer volume by dividing the
"excess PSA" by what is called the PSA leak associated with a Gleason
score of 6 (3+3). This would mean that your PC volume, assuming for a
moment a Gleason score of 6, would be excess PSA divided by the exact
PSA leak of 4.26 and the result is the cubic centimeters (cc) of the
tumors involved.
Table 1: PSA Leak vs Weighted Gleason Grade
Gleason Grade PSA leak
(Weighted) Rounded Off
5.0 1.0 (0.93)
4.5 1.5 (1.36)
4.0 2.0 (1.99)
3.5 3.0 (2.92)
3.0 4.0 (4.26)
2.5 6.0 (6.23)
2.0 10.0 (9.12)
1.5 15.0 (13.33)
1.0 20.0 (19.49)
With a Gleason grade of 4, we can presume a PSA leak of 2.0 and
recalculate the amount of PC as:
Excess PSA divided by PSA leak = calculated PC volume
Here you can see that the Higher the Gleason, the lower the PSA.
Pretty evident when a Gleason grade of 5 gives out only 23% of the
amount of PSA that is given with a Gleason grade of 3, A PSA of 2
with all grade 5 would be like a PSA of around 9 with all grade 3, but
FAR MORE AGGRESSIVE.
> 2) and these various growth rates plotted like a train schedule so you
> can predict how fast it's growing?
PSA doubling time (PSA velocity) gives you a way to track tumor
growth. You can convert it to tumor volume with the above algorithm.
Again, the assumption is that prostatitis or BPH are not playing a
role in the amount of PSA.
>3) and once it grows to a certain
> size, plot the spread rate of it metastasizing?
Again, some comments by Dr. Strum...
The next question is how high of a PSA can you have and have the tumor
restricted to the gland. I have seen a PSA of 64 that was reduced to
7 when the prostatitis was treated with long term Cipro (6 weeks). I
have seen reported PSA's as high as 100 from prostatitis. Otherwise
by far the most diagnosed cancer contained to the gland will have a
PSA of 10 or less and occasionally higher. But in all cases one must
consider BPH
and prostatitis.
Usually any PSA of above 20 - we consider that it may have
metastasized to the body and recommended various scans. The problem
with this number is that it may be caused by prostatitis or a large
amount of Gleason grade 3. With a Gleason Grade of only 3 and/or
prostatitis there would be no metastatic cancer. How can a doctor
recommend scans when he never checks why the PSA is over 20 - is there
BPH and /or prostatitis involved?.
>4) there are partin
> tables and other charts (?) but do these and other tables actually
> answer these questions of time?
The Partin tables are not time dependent.
>5) what effect are various well known
> supplements on the occurrence of the tumor?
This is an interesting one! If you look hard enough you can probably
find a study that says any supplement (flax seed oil, zinc, lycopene,
etc.) is bad for PCa. The conclusions of these studies are usually
only mildly indicative at best. There are a few supplements like
selenium, vitamins D and E, and fish oil for example, where it is
generally agreed that they offer some help in reducing the risk of PCa
in the first place, don't know about recurrences.
>6) what kind of life
> expectations beyond the five year mark are given for these predictions?
If you are asking does 10 year biochemical recurrence-free survival
data exist for various initial treatment options, then the answer is
yes for RP, EBRT and SI+EBRT. Peer reviewed published data exist for
the first two treatment methods, and an AUA poster abstract exists for
the third. I have provided references in some recent posts
> 7) once the prostate organ is gone, does this mean the cancer cells will
> grow at a different rate? remember once it does spread, they are still
> known as prostate cancer cells; that is prostate cancer of the bone not
> bone cancer. (there is something produced in the prostate that slows
> cancer growth)
It seems to be generally agreed that if the PCa has metastasized, and
the prostate is then surgically removed, then the growth rate at the
secondary sites increases. The discussion around this topic centers
on whether the increased growth rate is due to removal of control
factors provided by the primary tumor(s) or whether growth factors
which are produced in large amounts during the healing process are to
blame. Don't know if these arguments apply to other treatment
methods.
> here's my 1am thoughts,
> the growth rate of tumors. okay, 1st we know there is the gleason score
[quoted text clipped - 18 lines]
> bone cancer. (there is something produced in the prostate that slows
> cancer growth) hmm... things to ponder in the middle of the night, greg
Bill Denton - 29 Dec 2003 16:32 GMT
"3) and once it grows to a certain size, plot the spread rate of it
metastasizing?"
I don't think size is always the determinant. For example, a large,
aggressive tumor deep inside the prostate may have minimal metastatic
potential in the short term while a small one that has broken through
the capsule may already have spread its evil seeds.
"7) once the prostate organ is gone, does this mean the cancer cells
will
grow at a different rate? ...(there is something produced in the
prostate that slows cancer growth)"
Greg, knowingly or not, you've hit on one of the most interesting (to
me) theories of cancer progression. Dr, Judah Folkmann, who is
credited w/ the discovery of tumor angiogenesis (the formation of a
blood supply to the tumor), theorized that the primary tumor, e.g. PCa
in the prostate gland, secretes an angiogenesis inhibitor that keeps
distant metastases in check so the primary tumor has dibs on its
unfortunate victim. Think of a parasite-host relationship - the
parasite (PCa) does not want to kill the victim too quickly so it
keeps its lethal offspring at bay while it gets its fill. Thus, when
the primary tumor is removed or killed, there is no more angiogenesis
inhibotor and the dormant metastases wake up and start growing. You
probably know cancer patients who were thought not to be metastatic
who had primary treatment and w/i a short time they were in big
trouble and went downhill. That's the anecdotal evidence of the
theory. Now it's not all that simple because treatment based on
angiogenesis inhibitors like angiostatin did not work as expected, but
there still may be some validity to the theory. The obvious
implication would be not to treat primary tumors in cases of likely
metastasis, which is already pretty much the case but for different
reasons.
Bill Denton
RP 2/12/02
Memphis