Special Lady,
It is suspected that the age-related decline in T levels is the very reason that both incidence and virulence of PC increase as we age. The mechanism driving this has been investigated in lab studies, several of which show that normal T levels seem necessary to maintain apoptosis (lack of apoptosis is a hallmark of cancer.) One theory proposed by Richmond Prehn of UW is called "compensatory hyperplasia":
Prehn said...
A different hypothesis, that I shall put forward in this paper, is that declining androgen levels play a causative role in prostatic carcinogenesis. The hypothesis is based, in large part, upon the fact that prostatic-tumor incidence is the most age dependent of any tumor incidence: the incidence rises as the 9th or 10th power of age . Simultaneously, as individuals age and the risk of prostate cancer rises, the androgen levels fall. Thus, the older the individual, the greater is the risk of prostate cancer and the lower is the level of androgen, a relationship that argues that an unusually high androgen level may not be a causative factor in the origin of a prostate cancer. This relationship between prostate cancer and aging suggests that it may be a falling rather than an elevated level of androgen that facilitates prostate oncogenesis. The mechanism by which a falling androgen level may be instrumental in the genesis of prostate cancers probably involves compensatory hyperplasia.
On the Prevention and Therapy of Prostate Cancer by Androgen Administration- Allen