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PROTEUS SIGNED

Predicting Routes Of Tumour Evolution driven by Unstable genomes and Selection

Total Cost €

0

EC-Contrib. €

0

Partnership

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 PROTEUS project word cloud

Explore the words cloud of the PROTEUS project. It provides you a very rough idea of what is the project "PROTEUS" about.

describes    doubling    elevated    progress    newly    structural    evolutionary    immune    evolution    resistance    treatment    model    mutational    majority    sequence    survival    gin    barcode    longitudinal    incurable    cell    chromosomal    sensitive    generate    clinical    patient    surveillance    sufficiently    burden    genomic    multiple    lung    outcome    gd    heterogeneity    individual    outcomes    interactions    mouse    decipher    highlighting    underpinning    tumour    animal    somatic    quantifying    patterns    genome    metastatic    microenvironment    models    frequency    numerical    underlying    risk    dna    patients    therapy    fitness    macroevolutionary    histories    synthesise    copy    life    stratification    immunotherapy    encompassing    cancer    provides    poor    ith    instability    drug    describe    recapitulate    dynamics    small    aberrant    cin    nsclc    recurrence    tumours    tracerx    disease    evasion    cellular    death    diversity    unclear    substrate    immuno    solid    chemo    sequencing    micro    revealed    despite   

Project "PROTEUS" data sheet

The following table provides information about the project.

Coordinator
THE FRANCIS CRICK INSTITUTE LIMITED 

Organization address
address: 1 MIDLAND ROAD
city: LONDON
postcode: NW1 1AT
website: www.crick.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 2˙500˙000 €
 EC max contribution 2˙500˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-ADG
 Funding Scheme ERC-ADG
 Starting year 2019
 Duration (year-month-day) from 2019-06-01   to  2024-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE FRANCIS CRICK INSTITUTE LIMITED UK (LONDON) coordinator 2˙500˙000.00

Map

 Project objective

Despite progress in cancer drug development, the majority of patients who present with advanced, metastatic, solid tumours have incurable disease due to underlying cancer genomic diversity that provides a substrate for evolution and selection of drug resistance. The aim of this proposal is to describe, synthesise and model the micro- and macroevolutionary patterns of genomic instability underpinning the evolutionary dynamics of tumour life histories, to improve patient stratification, treatment and survival outcomes. Longitudinal clinical studies such as TRACERx are highlighting the complex processes that generate this intra-tumour heterogeneity (ITH). Genome Instability (GIN) describes aberrant changes within the genome, encompassing genome doubling (GD), numerical or structural chromosomal instability (CIN), and elevated DNA sequence mutational diversity. TRACERx has revealed that elevated DNA copy-number ITH rather than DNA sequence diversity is associated with increased risk of recurrence or death in non-small cell lung cancer (NSCLC). Why macroevolutionary CIN rather than somatic mutational diversity is associated with poor outcome remains unclear. Current animal models of NSCLC do not sufficiently model the multiple distinct patterns of GIN operating in patients. We aim to develop mouse lung cancer models that recapitulate the patterns of GIN observed in NSCLC patients. Using tumour barcode sequencing, a sensitive method of quantifying cellular fitness and individual tumour growth, we will investigate the effects of targeted-, chemo- and immuno-therapy on the newly generated GIN models. We will decipher if distinct patterns of GIN increase metastatic potential and treatment failure, and test if high mutational burden or high CIN increases the frequency of GD in cancer. Finally, we aim to investigate the effects of GIN upon immune surveillance, immune evasion, immunotherapy response, and the interactions between tumours and the tumour microenvironment.

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