By Shutsung Liao, John M. Kokontis, Chih-Pin Chuu, Richard A. Hiipakka (auth.), James Mohler, Donald Tindall (eds.)
This publication serves as a tribute to the paintings of the numerous investigators who've tried to appreciate the function of the androgen receptor (AR) within the improvement and development of prostate melanoma. the connection among prostate melanoma and androgen prestige was once first and foremost favored within the past due 1800’s, after which wisdom reawakened within the 1940’s by means of the reviews of Charles Huggins and associates, for which the Nobel prize used to be offered in 1966.
The goal of this ebook is to supply an up to the moment evaluate of the molecular and mobile elements of androgen motion in prostate melanoma. It comprises an summary of the position of androgens within the improvement of the traditional prostate and development of prostate melanoma. Our figuring out of androgen metabolism and efforts to focus on androgen metabolism within the prevention and remedy of prostate melanoma is gifted. Androgen receptor structure/function relationships and the position of co-regulators are outlined. Ligand-independent activation of the androgen receptor and the position of the androgen receptor in the course of development to the castration recurrent phenotype are mentioned. Androgen-regulated genes are elucidated and their roles in the course of prostate melanoma development are outlined. ultimately, the androgen receptor is gifted as a potential objective for novel treatments. jointly, those experiences may still provide the reader a accomplished conceptual framework of androgen motion in prostate cancer.
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Extra resources for Androgen Action in Prostate Cancer
1 nM R1881) that were optimal for 104-S cell proliferation. 1 nM R1881 (Kokontis et al. 1998). The original 104-R cells were referred to as 104-R1 cells. During the transition of 104-S cells to 104-R1 and 104-R2 cells, AR mRNA and protein level increased dramatically. AR transcriptional activity, measured by androgen induction of prostate-specific antigen (PSA) mRNA or expression of an androgen-dependent reporter gene transfected into cells, also increased up to 20fold during the progression. LNCaP 104-R1 and 104-R2 cells were proliferatively insensitive to the antiandrogen bicalutamide (Casodex).
1995). This process activates the second activation domain (AF-2) of AR. Differences in the ability of testosterone and dihydrotestosterone to activate AR may be related to differences in the ability of these ligands to modulate AF-2 activity (Askew et al. 2007). Cloning of the AR cDNA allowed us and many other investigators to define mutations in AR that are responsible for androgen-insensitivity in humans (Marcelli et al. 1990; Ris-Stalpers et al. 1990; Sai et al. 1990; Trifiro et al. 1991; McPhaul and Marcelli 1992; Bruggenwirth et al.
126:372–375. , Menke, J. , MacNaul, K. , Wright, S. , Sparrow, C. P. and Lund, E. G. 2001. 27-Hydroxycholesterol is an endogenous ligand for liver X receptor in cholesterolloaded cells. J. Biol. Chem. 276:38378–38387. , Kokontis, J. , Hiipakka, R. , Chuu, C. P. and Liao, S. 2004. Antiproliferative effect of liver X receptor agonists on LNCaP human prostate cancer cells. Cancer Res. 64:7686–7689. , Lin, T. , Sonnenschein, C. and Soto, A. M. 1997. Expression of novel genes linked to the androgen-induced, proliferative shutoff in prostate cancer cells.
Androgen Action in Prostate Cancer by Shutsung Liao, John M. Kokontis, Chih-Pin Chuu, Richard A. Hiipakka (auth.), James Mohler, Donald Tindall (eds.)