world cancer report - iarc

Indicator Number of oral contraceptive users among Relative risk (95% confidence interval)
androgen receptor with a four times higher
affinity than testosterone [18]. One determinant
of intra-prostatic dihydrotestosterone
formation may be variation in the
activity of intraprostatic (type II) 5-α-reductase
(SRD5A2), that catalyses the testosterone-dihydrotestosterone
conversion.
Another possible determinant, which could
provide a physiological link between
prostate cancer risk and nutritional lifestyle
factors, is an increase in circulating levels
of bioavailable testosterone unbound to sex
hormone binding globulin, that can freely
diffuse into the prostatic cells.
The androgen hypothesis originated from
80 The causes of cancer
Ovarian cancer cases Controls
Age (years)
< 45 48 221 0.6 (0.3-1.0)
45-54 30 92 0.5 (0.3-1.0)
55-64 2 11 0.6 (0.4-0.9)
Parity
0 21 67 0.6 (0.4-0.8)
1 15 75 0.6 (0.4-0.9)
≥ 2 44 182 0.3 (0.1-1.4)
Table 2.22 Estimated relative risk of ovarian cancer for women who have used oral contraceptives at any period in their lives, given for different ages and number
of births. S. Franceschi et al. (1991) Int J Cancer, 49: 61-65.
observations that surgical or medical castration
can often dramatically improve the
clinical course of advanced metastatic
prostate cancer patients. Furthermore,
Japanese and Chinese migrants to the USA
have lower incidence rates of prostate cancer
than men of African or European
ancestry, and at the same time have been
found to have lower 5-α-reductase activity;
there are positive associations of prostate
cancer risk with specific genetic polymorphisms
in the SRD5A2 gene. Finally, polymorphisms
in the androgen receptor gene
causing increased receptor transactivation
have also been found associated with an
increase in prostate cancer risk [12,19].
On the basis of the above observations,
one can predict an increase in prostate
cancer risk in men with elevated blood levels
of bioavailable testosterone, as well as
with levels of androstanediol-glucuronide,
a major breakdown product of dihydrotestosterone
and a possible marker of
intraprostatic androgen activity. These predictions,
however, have received only very
limited support from epidemiological studies
[20]. There is little evidence as yet for
any association between circulating estrogen
levels and prostate cancer risk.