Jan Trapman

TL;DR: In the LNCaP androgen receptor a single point mutation is discovered changing the sense of codon 868 (Thr to Ala) in the ligand binding domain, which influences both binding and the induction of gene expression by different steroids and antisteroids.

TL;DR: Investigation of effects of growth factors on stimulation of the AR-mediated gene transcription in human prostatic tumor cell lines provides evidence that IGF-I, KGF, and EGF directly activate the AR in the absence of androgens, which means that the androgen-signaling chain may be activated by growth factors in an androgens-depleted environment.

TL;DR: Failure of conventional androgen deprivation therapy in prostate cancer may be caused by a clonal expansion of tumor cells that are able to continue androgen-dependent growth despite of the low concentrations of serum androgens.

TL;DR: The androgen receptor is a member of the family of nuclear receptors that is able to regulate a specific expression of target genes and is expressed at high levels in male reproductive tissues.

TL;DR: A series of human androgen receptor (AR) deletion mutants was constructed to study the relationship between the structural domains and their different functions in the AR protein, indicating that in the absence of hormone this domain displays an inhibitory function.