CDELP

CHD1 Deletion: Implications to Outcome and Treatment in Prostate Cancer

 Coordinatore INSTITUTE OF CANCER RESEARCH - ROYAL CANCER HOSPITAL 

 Organization address address: Old Brompton Road 123
city: LONDON
postcode: SW7 3RP

contact info
Titolo: Ms.
Nome: Lydia
Cognome: Turner
Email: send email
Telefono: +44 20 7153 5219

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 231˙283 €
 EC contributo 231˙283 €
 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-IIF
 Funding Scheme MC-IIF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-04-04   -   2016-04-03

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTITUTE OF CANCER RESEARCH - ROYAL CANCER HOSPITAL

 Organization address address: Old Brompton Road 123
city: LONDON
postcode: SW7 3RP

contact info
Titolo: Ms.
Nome: Lydia
Cognome: Turner
Email: send email
Telefono: +44 20 7153 5219

UK (LONDON) coordinator 231˙283.20

Mappa


 Word cloud

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

comprising    prostate    etsnr    del    less    ets    ar    etsnrchd    repair    dna    rearranged    chd    etsr    cancers   

 Obiettivo del progetto (Objective)

'Prostate cancer can be stratified as ETS gene rearranged (ETSR) and non-rearranged (ETSNR), with the latter comprising a heterogeneous group of 50-60% of all cancers. This project will characterize a subgroup of ETSNR cancers that have a CHD1 deletion (CHD1del). Recent sequencing studies have elucidated CHD1- cancers as ETSNR, and commonly PTEN and p53 wildtype and SPOP mutated, comprising up to 26% of all prostate cancers (1). ETSR cancers largely have hormone driven oncogenes that may have prognostic and predictive utility (2, 3). Less is known about ETSNRCHD1del cancers. Their lack of ETS fusions raises concern that these may not be generated through androgen receptor (AR) transcription and are not AR driven. ETSNRCHD1del cancers have a huge excess of somatic intrachromosomal rearrangements (up to 800) compared to ETSR cancers presumably due to a DNA repair defect (1). This is supported by CHD1’s association with the SSRP1, part of the FACT complex, that is implicated in transcriptional regulation and DNA repair (4-9). We hypothesize that CHD1 deleted tumors are less sensitive to endocrine and taxane therapy, have a worse prognosis and need alternative treatment strategies.'

Altri progetti dello stesso programma (FP7-PEOPLE)

ADAPT_EVOL (2011)

The molecular process and functional consequences of adaptation

Read More  

TIFER (2011)

Tecnalia's International Fellowships for Experienced Researchers- TIFER

Read More  

LIPOGEST (2008)

Mechanisms by which interfacial layers control lipolysis on digestion

Read More