Can androgen receptor levels in the prostate predict non-organ-confined prostate cancer?

Freddie C Hamdy

This article has no abstract so we have provided the first paragraph of the full text.

Since the work of Charles Huggins over 50 years ago, androgen ablation remains the treatment of choice in men with metastatic prostate cancer. However, approximately 15% of patients will not respond to hormone manipulation, and the majority will relapse within 2–3 years of treatment. The mitogenic effects of androgens on prostatic growth are driven through the action of soluble peptide growth factors, acting in an autocrine or paracrine manner. These actions are mediated through the AR, a ligand-dependent transcription factor and member of the steroid/thyroid hormone receptor gene superfamily. Cellular signaling occurs following androgen binding to the AR and translocation to the nucleus. This activated complex associates with androgen-responsive elements contained in the DNA sequence of target genes, affecting the transcriptional activity of these genes. Mutations may result in changes in the function or expression of AR protein, or of growth factors and their receptors under the influence of AR coactivators, and AR amplification could lead to activation of the receptor by reduced levels of androgens.¹

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