Method based on surgery •
Orchiectomy (surgical castration) :It consists of removing the
testicles, the organ where
androgens are synthesized, of the cancer patient. It is the most radical treatment for ending the production of androgens. Moreover, it is the easiest and least expensive one. The main disadvantage is that surgical castration is a permanent method.
Methods based on drugs •
Chemical castration :The synthesis of
testosterone is mediated by a chain of processes that start in the brain. When the body detects a low level of testosterone, the
hypothalamus starts to produce
GnRH. GnRH activates the synthesis of
LH (Luteinizing hormone) within the pituitary gland. LH induces testosterone synthesis within the testicles. There are two different medicines,
GnRH agonists and
antagonists, which both lower the amount of testosterone made by the testicles. They work by inhibiting the formation of LH in the pituitary gland. The GnRH agonists produce a sudden increase on levels of testosterone followed by a huge falling, process called
flare, whereas GnRH antagonists decrease directly the amount of testosterone. GnRH agonists and antagonists used in androgen deprivation therapy include
leuprolide,
goserelin,
triptorelin,
histrelin,
buserelin, and
degarelix. :These drugs are injected under the skin achieving the same result as
surgical castration. Chemical castration may be preferred to surgical castration as it keeps the testes intact. •
Antiandrogen therapy :
Adrenal glands were discovered as another center of androgen production even after a castration process. Therefore a complementary treatment was developed that uses antiandrogens to block the body's ability to use any androgens. Prostate cells contain an androgen receptor (AR) that, when stimulated by androgens like testosterone, promotes growth and maintains prostatic differentiation. These pro-growth signals, however, can be problematic when they occur in a cancer cell. Antiandrogens can enter cells and prevent the binding of testosterone to the receptor proteins, due to their higher affinity for the androgen receptor. :The main antiandrogens are
cyproterone acetate,
flutamide,
nilutamide,
bicalutamide, and
enzalutamide which are all administered in oral tablet form. :New antiandrogens that target testosterone synthesis (
abiraterone acetate and
seviteronel) or AR nuclear translocation (
enzalutamide,
apalutamide, and
darolutamide), as well as combined therapies (
galeterone) have been recently developed and may function to better target androgen-responsive cells in combination with ADT. But these too may have negative adverse roles in the development of castration-resistant prostate cancer. ==Effects on male hormonal balance==