Nicola J. Clegg

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Metastatic prostate cancer is treated with drugs that antagonize androgen action, but most patients progress to a more aggressive form of the disease called castration-resistant prostate cancer, driven by elevated expression of the androgen receptor. Here we characterize the diarylthiohydantoins RD162 and MDV3100, two compounds optimized from a screen for(More)
Continued reliance on the androgen receptor (AR) is now understood as a core mechanism in castration-resistant prostate cancer (CRPC), the most advanced form of this disease. While established and novel AR pathway-targeting agents display clinical efficacy in metastatic CRPC, dose-limiting side effects remain problematic for all current agents. In this(More)
Activation of the androgen receptor is crucial for prostate cancer growth at all points of the illness. Current therapies targeting the androgen receptor, including androgen-depletion approaches and anti-androgens, do not completely inhibit the receptor activity. Prostate cancer cells develop resistance to castration by acquiring changes that include(More)
MYC and phosphoinositide 3-kinase (PI3K)-pathway deregulation are common in human prostate cancer. Through examination of 194 human prostate tumors, we observed statistically significant co-occurrence of MYC amplification and PI3K-pathway alteration, raising the possibility that these two lesions cooperate in prostate cancer progression. To investigate(More)
Nicola J. Clegg, John Wongvipat, Jim Joseph, Chris Tran, Samedy Ouk, Anna Dilhas, Yu Chen, Kate Grillot, Eric D. Bischoff , Ling Cai, Anna Aparicio, Steven Dorow, Vivek Arora, Gang Shao, Jing Qian, Hong Zhao, Guangbin Yang, Chunyan Cao, John Sensintaffar, Teresa Wasielewska, Mark R. Herbert, Celine Bonnefous, Beatrice Darimont, Howard I. Scher, Peter(More)
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