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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.

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

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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