Modeling AIPC using LNCaP cell lines and actual tissue from AIPC patients, Wang et al., 2009 found that the of gene expression regulated by the AR in the absence of hormone is distinct from androgen-regulated program and can selectively and directly upregulate M-phase genes found in androgen-independent CaP and may explain why maximal androgen deprivation, and cannot prolong androgen-independent survival. Most recently, it was found that overexpression of AR was a result to prolonged exposure of LNCaP-derived xenografts with the antiandrogen enzalutamide, and was similar to chronic androgen depletion, as a significant mechanism for drug resistance and CRPC development. In this study we characterized whole mutant AR protein complexes with several classes of steroids and ligands known to bind T877A-AR. The specific interactomes were dependent on the ligand utilized; so too were the specific gene expression profiles associated with each ligand. Thus mutant AR gain-of-function properties are not singular but multiple, dictated by the class of steroid hormones used. Further exploration of other adrenal androgens such as DHEA or androstenedione or other antiandrogens such as flutamide and bicultamide were not examined in this study, however, we did select a diverse class of ligands known to bind to the T877A-AR variant. High-throughput gene expression microarray approaches described in CaP cells have identified hundreds of and rogen regulated genes and also characterized genome-wide AR recruitment sites. The Pseudolaric-acid classical AR complex contains general transcription factors, coregulators and specific transcription CP-456773 sodium salt factors that associate either directly or indirectly with the AR to enhance or repress its transcriptional activity function without themselves necessarily binding to DNA. As shown in our recent proteomic studies, including this one, AR complexes may also include a larger number of functionally diverse proteins involved in a multitude of ����non-classical���� AR cellular processes such as histone acetylation, DNA methylation, ubiquitination, RNA splicing, apoptosis, and protein synthesis, with all pathways found to be dependent on hormone stimulation conditions.