Prostate tumors, although initially androgen dependent, inevitably progress
to a hormone-independent phenotype after treatment with androgen deprivati
on, This change in phenotype is a result of the selective growth of androge
n-independent cells already present at the initiation of therapy. The exact
mechanism by which an androgen-resistant cell develops is unknown. Potenti
al mechanisms involve alterations of the androgen receptor, gene amplificat
ion, altered signaling pathways, or aberrant expression of growth factors,
None of these alterations has been demonstrated universally in androgen-res
istant tumors. Most likely, it is the accumulation, as well as yet to be de
scribed synergism, of multiple genetic alterations that leads to the androg
en-resistant phenotype.