ARKSS

A large-scale siRNA screen to study the role of kinases in Androgen Receptor activation

 Coordinatore KOC UNIVERSITY 

 Organization address address: RUMELI FENERI YOLU SARIYER
city: ISTANBUL
postcode: 34450

contact info
Titolo: Mrs.
Nome: Askim
Cognome: Demiryurek
Email: send email
Telefono: +90 212 3381333
Fax: +90 212 3381205

 Nazionalità Coordinatore Turkey [TR]
 Totale costo 75˙000 €
 EC contributo 75˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2011-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-03-01   -   2015-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KOC UNIVERSITY

 Organization address address: RUMELI FENERI YOLU SARIYER
city: ISTANBUL
postcode: 34450

contact info
Titolo: Mrs.
Nome: Askim
Cognome: Demiryurek
Email: send email
Telefono: +90 212 3381333
Fax: +90 212 3381205

TR (ISTANBUL) coordinator 75˙000.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

screen    resistant    almost    androgen    patients    castrate    recurrent    kinases    cancer    treatment    genome    signaling    activation    prostate    kinase    ar    diagnosed   

 Obiettivo del progetto (Objective)

'Prostate cancer is one of most commonly diagnosed cancer in European men and a leading cause of cancer-related death. If the cancer is diagnosed early, it is frequently curable by surgery or radiotherapy. However, locally advanced, recurrent or metastatic prostate cancer is much more difficult to control. These patients are commonly treated with androgen withdrawal therapy that is designed to inhibit the activation of the androgen receptor (AR). While initially successful, the effectiveness of this type of treatment is usually temporary and the surviving tumour cells almost always progress to a “castrate-resistant ” state. The treatment options for these patients are very limited and the median patient survival is 1-2 years. Despite this resistance, there is considerable evidence that the inappropriate activation of AR is linked to recurrent cancer growth. The AR therefore, remains the most effective therapeutic target to treat castrate-resistant prostate cancer.

Phosphorylation of the AR by kinases has been demonstrated to induce transcriptional activation in low-androgen environments. This kinase-mediated pathway is believed to be one of the main causes of AR activation in castrate-resistant cancer patients. While various kinases have been identified to be involved in AR signaling, those tested only represent a small fraction of the total kinases present in the eukaryotic genome. Therefore, to better understand the role of kinases in AR activation, I am proposing to conduct a high-throughput siRNA screen against almost every kinase in the genome. This study will allow for the identification of those kinases that are critical for AR signaling. Importantly, this functional genomic screen will be conducted in multiple cell lines to give a deeper understanding of this heterogeneous disease. Given the importance of kinases of AR activation, the “hits” identified from this screen will offer novel drug targets for the treatment of prostate cancer.'

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