In Dr. Strum's book they show scans of PCa mets patients, whom after doing HT therapies the later scannings showed dramatic reductions and less visible mets found, thus it must be dimishing the amount of PCa cells.
Also, DES and other estrogenic drugs (estradiol patches or gels, or emcyt) can have a direct apoptosis effect on PCa cells, even some hprca cells as mentioned in this article from 2003 Journal of Urology, link also to be posted herein to the whole abstract, mentioning superior results over bicalutimide, bone improvement vs. losses from other HT therapies and cognitive pluses for estrogens too.
Diethylstilbestrol has been found to have in vitro cytotoxicity
against prostate cancer cell lines at physiological doses.
9, 56 In these studies DES was the active metabolite that
induced the cytotoxic effects seen in vitro.9 It has also been
demonstrated that DES has antitumor activity in previously
orchiectomized individuals with recurrent prostate cancer,
likely mediated through its ability to induce apoptosis in
hormone insensitive cells.8 In fact, the induction of apoptosis
by DES is somewhat dependent on the androgen sensitivity
state of the prostate cancer cell. Androgen insensitive prostate
cancer cells were more susceptible to apoptotic induction
by DES than androgen sensitive cells.8 This effect is not
mediated through the estrogen receptor, but involves alternative
mechanistic pathways. DES is also known to have a
direct antimicrotubular effect on prostate cancer.57, 58 It is
these direct effects that help explain the benefits (decreasing
prostate specific antigen) of 1 mg DES when patients treated
by LH-RH agonists/orchiectomy have disease relapse. Therefore,
castrate levels of testosterone may not be necessary in
men on DES treatment for prostate cancer.
Link abstract:
www.ffyates.com/prostate/des.pdf