Androgen resistance - clinical and molecular spectrum

Article Abstract:

Resistance to the activity of the male hormones (androgens) can interfere with normal male sexual development before birth and during puberty, and can cause infertility. The androgen hormones testosterone and dihydrotestosterone regulate development of the male genitalia before birth and secondary sexual characteristics during puberty, hormone production and sperm production. Mutations in single genes cause androgen resistance syndromes. The molecular defects that result from these mutations and cause androgen resistance are either deficiency of the enzyme 5-alpha-reductase or abnormalities in the androgen receptor. Individuals with 5-alpha-reductase deficiencies are not born with normal male genitalia and are often thought to be female. Mutations in the androgen receptor cause three types of abnormal androgen binding: no androgen binding, qualitatively abnormal binding and decreased but qualitatively normal binding. Individuals with this type of disorder have a wide range of abnormalities of their sexual characteristics and can appear to be male or female.

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Hyperandrogenism - what is normal?

Article Abstract:

Androgens are male hormones that are usually present at low levels in healthy women. Androgens are produced by the ovaries and adrenal glands. Excess facial and body hair and/or irregular or decreased menstruation are considered indicators of excessively high levels of androgens, or hyperandrogenism. Deficiencies of different adrenal gland enzymes can cause hyperandrogenism. Women suspected of having these deficiencies can undergo diagnostic testing. Hyperandrogenism caused by the ovaries is more difficult to diagnose and evaluate. A research study found that ovarian and adrenal gland hyperandrogenism are both common. Ovarian and adrenal gland hyperandrogenism may be caused by abnormalities in the same group of enzymes. Hyperandrogenism is partially defined in cultural terms. In some cases, women with higher levels of androgens do not need treatment. Others may need to be evaluated more carefully, and undergo treatment for an underlying disease such as cancer.

Ovaries, Adrenal glands

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The promiscuous receptor: prostate cancer comes of age

Article Abstract:

Scientists have long known that testosterone can stimulate the prostate gland, and consequently, castration has been a common treatment for prostate cancer. However, many prostate tumors continue to grow even after castration, a condition called androgen independence. A 1995 study revealed that metastatic prostate cancer bone marrow samples that grew in the absence of androgens contained a mutation in the androgen receptor gene. In some cases, the mutation was in the part of the receptor that binds androgens, and it caused the receptor to become sensitive to female hormones. Female hormones can also stimulate tumor growth, which could explain why these prostate tumors continued to grow. A more effective treatment for prostate cancer may involve reducing androgen levels and removing the man's adrenal glands, which produce steroid hormones.

Genetic aspects, Prostate cancer, Cell receptors

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