What exactly does this have to do with the androgen receptor, specifically? Not asking this sarcastically...
This has to do with silencing of AR signal, which is the basis of the androgen insensitivity theory
. It has been proposed by scientists that drug induced persistent side effects are due to epigenetic changes in gene expression levels, specifically by DNA methylation. Note that this paper
specifically talks about isotretinoin (Accutane, also a 5ARI class drug) as causing such problems. I had contact with the author of this paper and he also suspects finasteride as causing such problems.
Hence the idea about reversing this with a demethylating agent. Fortunately for us, many cancer forms are associated with hypermethylation of certain DNA segments. As most research $$ go into cancer research these days, we can hope that therapy options coming out of there could be useful to us.
My thoughts on this: Perhaps the root-root cause of our problem is an overactive Methyltransferase enzyme, which goes about hypermethylating DNA more actively than it should. Proof of this would be an unusual high incidence of cancer cases with persons in our blood line (parents, brother, sister, grandparents, cousins). Does that fit anyone?
Following quote gives the link with AR silencing further credence:
methylation of the androgen receptor promoter CpG island is associated with loss of androgen receptor expression in prostate cancer cells. The demethylating agent 5-aza-2′ deoxycytidine induced a re-expression of AR RNA (http://www.ncbi.nlm.nih.gov/sites/pubmed/9850055
5-aza-2 is a commercially available under the brand name Dacogen: http://www.cancer.gov/cancertopics/drug ... decitabinehttp://en.wikipedia.org/wiki/Decitabine