| Literature DB >> 16986004 |
Abstract
New developments in molecular and cellular biology are rapidly increasing knowledge of the mechanisms of androgen action in the prostate. Molecular profiling of recurrent cancer after androgen deprivation therapy has revealed genetic changes related to cell survival and proliferation. It is now clear that loss of the androgen receptor (AR) does not explain androgen-independent growth of a majority of recurrent cancers. Rather, overexpression, mutation, and ligand-independent activation of the AR may confer enhanced sensitivity to androgen or other growth factors. Therefore, the term "androgen-independent" is often a misnomer. This emerging concept is the basis of novel strategies to prevent or slow recurrence.Entities:
Year: 2001 PMID: 16986004 PMCID: PMC1476082
Source DB: PubMed Journal: Rev Urol ISSN: 1523-6161