ASPIRE-PC

A novel Androgen Synthesis Pathway in treatment-REsistant Prostate Cancer

 Coordinatore THE UNIVERSITY OF BIRMINGHAM 

 Organization address address: Edgbaston
city: BIRMINGHAM
postcode: B15 2TT

contact info
Titolo: Mr.
Nome: Xavier
Cognome: Rodde
Email: send email
Telefono: 441214000000
Fax: 441214000000

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 110˙803 €
 EC contributo 110˙803 €
 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-2013-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-03-01   -   2015-07-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF BIRMINGHAM

 Organization address address: Edgbaston
city: BIRMINGHAM
postcode: B15 2TT

contact info
Titolo: Mr.
Nome: Xavier
Cognome: Rodde
Email: send email
Telefono: 441214000000
Fax: 441214000000

UK (BIRMINGHAM) coordinator 110˙803.20

Mappa


 Word cloud

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

castration    receptor    intratumoral    dht    cancer    testosterone    pathway    synthesis    ar    pc    treatment    despite    crpc    androgen    activation    alternative   

 Obiettivo del progetto (Objective)

'Prostate cancer (PC) is the most prevalent non-cutaneous cancer in men and leads to high morbidity and mortality. Disseminated PC is treated by hormonal treatment in order to block intratumoral activation of the androgen receptor (AR) by 5α-dihydrotestosterone (DHT). Despite this treatment, eventually all patients develop castration-resistant disease (CRPC) which is accompanied by poor prognosis. Novel androgen synthesis and receptor inhibitors improve patient survival in CRPC, demonstrating the crucial role of residual androgen presence in PC despite castration. Besides the classic DHT synthesis pathway through testosterone, recent studies in humans have shown formation of DHT through an alternative pathway that does not require testosterone as an intermediate. Activity of this alternative androgen synthesis pathway is dependent on the presence of specific steroidogenic enzymes. Results of preliminary preclinical and clinical research show that levels of alternative pathway intermediates are increased in CRPC. Our goal is to investigate the activity and relevance of this novel pathway during progression of PC. The contribution of the alternative pathway to DHT-initiated AR activation will be explored using previously established in vitro models and sensitive steroid detection methods. This translational study will serve to discover novel targets for inhibition of intratumoral DHT synthesis and subsequent (CR)PC growth.'

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