@article {WINTERS3385, author = {BRIAN WINTERS and LISHA BROWN and ILSA COLEMAN and HOLLY NGUYEN and TSION ZEWDU MINAS and LORI KOLLATH and VALERI VASIOUKHIN and PETER NELSON and EVA COREY and AYKUT {\"U}REN and COLM MORRISSEY}, title = {Inhibition of ERG Activity in Patient-derived Prostate Cancer Xenografts by YK-4-279}, volume = {37}, number = {7}, pages = {3385--3396}, year = {2017}, publisher = {International Institute of Anticancer Research}, abstract = {Background/Aim: The aim of the current study was to determine the effects of the ERG small-molecule inhibitor YK-4-279 on ERG+ prostate cancer patient-derived xenografts (PDX). Materials and Methods: ERG activity was blocked using YK-4-279 in three subcutaneously-implanted ERG+ (LuCaP 23.1, 86.2 and 35) and one ERG- (LuCaP 96) PDX. Treated animals tumor volume (TV), body weight (BW) and serum prostate-specific antigen (PSA) were compared to vehicle-treated control animals. Gene expression, proliferation, apoptosis, microvessel density and ERG expression were also assessed. Results: Administration of YK-4-279 decreased TV (p=0.026), proliferation (p=0.0038) and PSA (p=0.022) in Severe Combined Immunodeficiency (SCID) mice bearing LuCaP 23.1 tumors. LuCaP 86.2, LuCaP 35 and LuCaP 96 showed no significant changes in TV, or PSA. Mineralocorticoid receptor (MR) and MR-direct target genes were up-regulated in treatment-resistant LuCaP 86.2 and LuCaP 35 PDX. Conclusion: YK-4-279 decreased ERG+ LuCaP 23.1 tumor growth, but not LuCaP 86.2 and LuCaP 35 ERG+ tumor growth.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/37/7/3385}, eprint = {https://ar.iiarjournals.org/content/37/7/3385.full.pdf}, journal = {Anticancer Research} }