Sorry I didn't answer this part in my previous post.  If my model is
correct, then it is possible to construct a genetic makeup for PCa
that will either have increased cell growth or increased cell death
depending on the makeup of the hormone receptors.  This is because for
each of the hormones (testosterone, progesterone, and estradiol) there
are two receptors acting in opposition to each other.  In reality, for
men with normal genetic makeup, all of the hormones initially increase
the rate of cell death.  If their levels are high enough, e.g. a
typical teenage level, then PCa can not proliferate.  As men age, and
the hormone levels drop, then PCa can start up.  Once it starts up,
Darwinian evolution occurs, and each mutation that protects it from
the hormones has a selective growth advantage.  By the time a man
becomes terminal, it is likely that the PCa will increase its growth
rate in response to each of the three main hormones.  So to answer
your question, in theory it is possible to have PCa cells die solely
by using hormones, but in practice in will never happen unless you can
start increasing hormone levels at the point that there is only a few
cancer cells and no mutations yet.

On another note, there seems little doubt that the initiating step in
causing PCa is high local levels of estradiol (same for breast
cancer).  Continual high levels of estradiol immortalize those cells
by producing oncogenes such as Myb which cause the cells to divide and
producing telomerase which allows the cells to divide without
shortening their telomeres.  However, even though this initiates PCa,
the hormone levels (especially T) must be low enough in order for PCa
to proliferate.

Also, to clarify a bit the difference between my view on PCa and that
of the Bruchovsky paper is that in their paper every time they applied
ADT and the tumor shrank, they said it's not AI yet.  When it finally
does become AI, they try to figure out why it became so on that
particular round of intermittent ADT.  From my point of view, every
time they apply ADT, they are killing many cells, freeing up the
existing AI cells to grow more freely without the constraint found by
cells in the interior of a tumor trying to multiply (usually only the
outer edge of the tumor freely multiplies).  Also, some cells will
have a growth rate slightly less than their rate of cell death, and
each round of ADT will have less and less of those cells.  There are
also some cells that have a growth rate slightly greater than their
rate of death, and they will coexist with the AI cells once the tumor
is officially declared to be AI.

Ed Friedman