Dick, As one has has an aggresive strain, my thoughts are.......

Step out of the box or circle. Don't look at PCa as most Ca. Very rarely
will one ever "see" tumors per se. Think of micro fibers floating through
your blood system endlessly until they want to stop and feed; attaching
themselves to some part of your body that needs blood supply. Think away
from vessels and think at bone or soft-tissue.

After attaching, the micro fibers grows to where it can now be seen.
Typically, seen when the damage starts to show.

The real problem is that once the micro fibers escape, it does not matter
what your primary treatment was.... removal, internal radiation, or external
radiation.... it is too late. You simply can not know or detect or that Ca
lives somewhere in your body ready to start its life cycle.

When I started down this path, I was given a 92% shot of not having a micro
fiber escape. I simply feel into the 8% group.

Mike

Mine was a Gleason 8 with seminal vesicle involvement and a PSA velocity >
2.0 (which increases by a thousand percent my odds of dying OF PCa,
according to a recent study). My oncs recommended ADT immediately following
my RRP, because ADT fights PCa body-wide rather than just in the prostate
bed and has the greatest chances of success when the target cell population
is at its smallest. They didn't bring up the topic of adjuvant RT until we
began discussing what to do if and when my cancer returns, apparently
favoring RT after some significant time has gone by (my RRP was a year ago).

I'll start researching RT a whole lot further when my PSA starts up again,
but I've already done enough research on it to know I wouldn't take it just
because a doctor recommends it. Like the other treatments, it has its own
suite and likelihood of SEs., and I want to evaluate them under the light of
my own suite of priorities.

I.P.

It has been discussed.  Has been tried and been reported on.  It is more
successful regarding percentages, but the percentages were inconclusive as
to warrant putting men through all the RT SEs.  Most docs are (and I think
should be) discriminating.

There have been some studies, but I think it is still not clear.

I have read that some doctors do advocate scheduling RT after
RP without waiting for PSA to climb.  However I believe that even
they want to wait for the surgical wounds to heal before radiation
so as not to impose crippling damage on the patient.

It seems to me that there are several separate aspects to
your question.

1. Is RT necessary?

Even though the cancer was aggressive, what if the surgery
got all of it?  If it did, then enduring the radiation would be
entirely unnecessary.  If we don't wait for PSA to rise, we
don't know if we actually needed radiation and we'd risk
accepting all of the side effects of RT for no benefit.

2. Is RT more effective if given right away, without waiting for
   PSA to rise?

This is a tough one.  We do know that RT is more effective
earlier than later.  We do know that the chances for metastasis
increase with time.  But we also know that tumor growth is
generally accompanied by a rise in PSA.  So the question
is, is a rise in PSA a "leading" or "trailing" indicator of
cancer progression that might not be treatable by RT?

If it's a leading indicator, then we can wait for a rise in PSA
before radiating.  If it's a trailing indicator, then when the PSA
rises, it's too late.

It seems to me that the answer to that question is not known
with certainty.  We do know of men on this newsgroup and
reported in studies who have had RP, had a rise in PSA, had
RT, and the PSA rise stopped.  So, at least for some men,
a rise in PSA signalled a cancer progression that could still
be stopped by RT.

However we also know that there are some men in the
newsgroup who had a fairly small rise in PSA, got radiation,
and did not see their cancer progression halted.

But even for those guys, we still don't know if RT before the
rise in PSA would have helped them.  It's entirely possible
that if they had gotten RP and RT on the same day, they
still wouldn't have gotten all the cancer because some had
already established itself outside the treatable zone, or
because some was somehow radiation resistant.

So I'm thinking that the answer to your question is that the
desirability of RT post RP but before a rise in PSA probably
differs for different specific cases, and nobody has a sure
way to tell if it will help.

The solution that most doctors seem to adopt - wait for a rise
in PSA before prescribing RT - seems reasonable in light of
all the unknowns.  However, if the pre-RP diagnosis was of
an aggressive cancer, I would think an aggressive PSA testing
schedule is desirable to catch any rise in PSA as early as
possible.

    Alan

Postoperative radiotherapy after radical prostatectomy: a randomised
controlled trial (EORTC trial 22911).

Bolla M, van Poppel H, Collette L, van Cangh P, Vekemans K, Da Pozzo L, de
Reijke TM, Verbaeys A, Bosset JF, van Velthoven R, Marechal JM, Scalliet P,
Haustermans K, Pierart M; European Organization for Research and Treatment
of Cancer.

Department of Radiation Oncology, Centre Hospitalier Universitaire A
Michallon, Grenoble, France. MBolla@chu-grenoble.fr

BACKGROUND: Local failure after prostatectomy can arise in patients with
cancer extending beyond the capsule. We did a randomised controlled trial to
compare radical prostatectomy followed by immediate external irradiation
with prostatectomy alone for patients with positive surgical margin or pT3
prostate cancer. METHODS: After undergoing radical retropubic prostatectomy,
503 patients were randomly assigned to a wait-and-see policy, and 502 to
immediate postoperative radiotherapy (60 Gy conventional irradiation
delivered over 6 weeks). Eligible patients had pN0M0 tumours and one or more
pathological risk factors: capsule perforation, positive surgical margins,
invasion of seminal vesicles. Our revised primary endpoint was biochemical
progression-free survival. Analysis was by intention to treat. FINDINGS: The
median age was 65 years (IQR 61-69). After a median follow-up of 5 years,
biochemical progression-free survival was significantly improved in the
irradiated group (74.0%, 98% CI 68.7-79.3 vs 52.6%, 46.6-58.5; p<0.0001).
Clinical progression-free survival was also significantly improved
(p=0.0009). The cumulative rate of locoregional failure was significantly
lower in the irradiated group (p<0.0001). Grade 2 or 3 late effects were
significantly more frequent in the postoperative irradiation group
(p=0.0005), but severe toxic toxicity (grade 3 or higher) were rare, with a
5-year rate of 2.6% in the wait-and-see group and 4.2% in the postoperative
irradiation group (p=0.0726). INTERPRETATION: Immediate external irradiation
after radical prostatectomy improves biochemical progression-free survival
and local control in patients with positive surgical margins or pT3 prostate
cancer who are at high risk of progression. Further follow-up is needed to
assess the effect on overall survival.

I was diagnosed with agressive PCa after LRP.  After a recovery period
I was started on one year of HRT(Lupron) and EBRT without waiting on
PSA to rise.

Roy