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DiSect SIGNED

The Tumour Stroma as a Driver of Clonal Selection

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 DiSect project word cloud

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

1r    stroma    elicit    treatment    expressed    homogeneous    characterised    cell    simultaneously    delineating    suppressors    vitro    genetic    appreciate    driver    accumulation    undertaken    pancreatic    context    proteomics    krasg12d    critical    engage    differ    frequent    co    axl    kras    ductal    signal    drive    interaction    display    therapies    expressing    fibroblasts    immune    shown    surveillance    reciprocal    tumorigenic    tp53    global    opt    mutations    cultures    igf    specificity    phosphoproteomics    autonomous    signals    combination    accompanied    cancer    discern    adenocarcinomas    smad4    regulates    incompletely    clonal    resistance    stages    receptor    infiltrating    previously    gradual    host    extensive    combine    tumours    oncogenic    stromal    cdkn2a    recruit    tumour    heterocellular    evasion    labelling    pda    computational    kinases    pro    tyrosine    additional    desmoplasia    cells    progression    signalling    activated    loops    interact    directionality    actively    activate    restrictive    aberrations    interactions   

Project "DiSect" data sheet

The following table provides information about the project.

Coordinator
THE UNIVERSITY OF MANCHESTER 

Organization address
address: OXFORD ROAD
city: MANCHESTER
postcode: M13 9PL
website: www.manchester.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 1˙969˙768 €
 EC max contribution 1˙969˙768 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-COG
 Funding Scheme ERC-COG
 Starting year 2018
 Duration (year-month-day) from 2018-06-01   to  2023-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF MANCHESTER UK (MANCHESTER) coordinator 1˙969˙768.00

Map

 Project objective

Pancreatic ductal adenocarcinomas (PDA) are complex heterocellular tumours characterised by extensive desmoplasia. Tumour and stromal host cells actively engage to establish reciprocal signalling loops, which drive cancer progression, resistance to treatment and evasion of immune surveillance. However, the specificity and directionality of these interactions are incompletely characterised. We have previously shown that tumour cells expressing the main oncogenic driver (KRASG12D) co-opt stromal fibroblasts to elicit a reciprocal signal, which activate tumour cell IGF-1R and AXL receptor tyrosine kinases. Importantly, these signals enable tumour cells to engage additional signalling pathways not activated when oncogenic KRAS is expressed in homogeneous tumour cell cultures. Therefore, to fully appreciate tumour cell signalling, studies should be undertaken within the context of the tumour stroma. Early stages of PDA display a gradual accumulation of mutations where activated KRAS is accompanied by loss of tumour suppressors CDKN2A, TP53 and SMAD4. Simultaneously, there is an accumulation of infiltrating stromal cells. To address how PDA cells differ in their interaction with the infiltrating stroma, we will use in vitro co-cultures to study how PDA cells with frequent genetic aberrations recruit and interact with host stromal cells. We will combine our unique methodologies for cell-specific labelling with global proteomics and phosphoproteomics analysis to discern cell-specific signalling between tumour and stroma cells. Following, we will analyse the impact of the tumour stroma on clonal selection and use computational modelling to identify which cell autonomous and non-cell autonomous signals drive progression. Delineating how reciprocal signalling regulates early tumour cell signalling and clonal selection is critical to define pro-tumorigenic from restrictive stromal elements in order to improve combination therapies.

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