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Silvia Ottaviani, Alexander de Giorgio, Victoria Harding, Justin Stebbing and Leandro Castellano

transcriptional output from miRNA loci. Expression profiling studies in prostate cancer have identified an array of androgen up- and down-regulated miRNAs potentially involved in prostate cancer progression ( Porkka et al . 2007 , Ambs et al . 2008 , Ozen et

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Laurent Léotoing, Michèle Manin, Didier Monté, Silvère Baron, Yves Communal, Corinne Lours, Georges Veyssière, Laurent Morel and Claude Beaudoin

-responsive mesenchyme in the prostate can elicit a tissue-specific morphologic development of the epithelium, assessed to be negative for AR expression ( Cunha 1996 ). Altogether, these findings suggest that androgen-induced epithelial cell proliferation in the male

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Felix F Brockschmidt, Markus M Nöthen and Axel M Hillmer

, Lundin et al. (2007) reported the first functional comparison of AR with polyG23 and polyG24 using a prostate-specific antigen promoter-driven reporter gene in COS-1 cells. PolyG23 showed higher transactivating activity than polyG24 at various DHT and

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Valeria Giandomenico, Tao Cui, Lars Grimelius, Kjell Öberg, Giuseppe Pelosi and Apostolos V Tsolakis

human OR51E1. OR51E1 mRNA expression has been detected in normal brain ( Vanti et al . 2003 ) and prostate tissue ( Weigle et al . 2004 ). Furthermore, cancer cells, such as prostate carcinoma cells ( Weigle et al . 2004 , Fuessel et al . 2006

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Xiang Zhang and Shuk-Mei Ho

genes in prostate cancer. Intratumoral testosterone levels were found to be higher in metastases removed from castrated men than in primary prostate cancer from untreated eugonadal men. The ability of the cancer to survive and progress to a higher grade

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R Urbatzka, B Watermann, I Lutz and W Kloas

mammals, as in amphibians, the more potent androgen is DHT unlike in fish, where 11-ketotestosterone is the most potent androgen ( Norris 1997 ). DHT promotes in humans and mammals the development of external genitalia or androgenic tissues like prostate

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Misa Nakamura, Bo Han, Toshihide Nishishita, Yanhua Bai and Kennichi Kakudo

found that CT suppresses constitutive phosphorylation of extracellular signal-regulated kinase (ERK1/2) in DU145 prostate cancer cells ( Segawa et al . 2001 ). However, the precise pathways involved are currently unclear. The purpose of this study was

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Sang R Lee, Mi-Young Park, Hyun Yang, Geun-Shik Lee, Beum-Soo An, Bae-kuen Park, Eui-Bae Jeung and Eui-Ju Hong

proliferation and hypertrophy in the prostate, whereas they are only involved in cell hypertrophy in the kidney ( Catterall et al . 1986 ). Although kidneys do not require androgens for normal functions ( Catterall et al . 1986 ), it is possible that androgens

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Rosalia C M Simmen, Melissa E Heard, Angela M Simmen, Maria Theresa M Montales, Meera Marji, Samantha Scanlon and John Mark P Pabona

disease, namely prostate cancer, is also highly associated with dysfunctions in numerous KLFs including KLF4 ( Wang et al . 2010 ), KLF5 ( Frigo et al . 2009 ), KLF6 ( Narla et al . 2001 ), KLF8 ( He et al . 2013 ), and KLF9 ( Shen et al . 2014

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J Jääskeläinen, A Deeb, J W Schwabe, N P Mongan, H Martin and I A Hughes

with PAIS ( Ahmed et al. 2000 ) but also as a somatic mutation in prostate cancer ( Takahashi et al. 1995 ). As in our patient, this mutation leads to decreased androgen binding affinity, evidenced by high K d in several reports. Substitution of