Some prostate cancers are highly dependent upon androgens for cellular proliferation; therefore, physicians attempt to totally ablate the secretion of androgens by the testes. Generally, two options for those patients are surgical castration and chemical castration. Surgical castration is irreversible and requires the removal of the testes, while chemical castration is reversible.
One option for chemical treatment of these patients is the use of analogs of GnRH, the hormone that regulates the secretion of LH and FSH. Long-acting GnRH agonists or antagonists reduce LH and FSH secretion by different mechanisms. GnRH agonists reduce gonadotropin secretion by desensitization of the pituitary gonadotrophs to GnRH, leading to a reduction of LH and FSH secretion. GnRH agonists initially stimulate GnRH receptors on pituitary cells and ultimately reduce their numbers. GnRH antagonists bind to GnRH receptors on the pituitary cells, prevent en-
dogenous GnRH from binding to those receptors, and subsequently reduce LH and FSH secretion. Shortly after treatment, testicular concentrations of androgens decline because of the low levels of circulating LH and FSH. The expectation is that androgen-dependent cancer cells will cease or slow proliferation and, ultimately, die.
GnRH agonists (leuprolide acetate [trade name Lupron]) are usually used in combination with other drugs in order to block most effectively androgenic activity. For example, one of the androgen-blocking drugs includes 5a-reductase inhibitors that prevent the conversion of testosterone to the highly active androgen dihydrotestosterone (DHT). In addition, antiandrogens, such as flutamide, bind to the androgen receptor and prevent binding of endogenous androgen. Some prostate cancers are androgen-independent, and the treatment requires nonhormonal therapies, including chemotherapy and radiation.
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