CDELP

CHD1 Deletion: Implications to Outcome and Treatment in Prostate Cancer

Coordinatore	INSTITUTE OF CANCER RESEARCH - ROYAL CANCER HOSPITAL    more  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.

 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.'