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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.

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

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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The information about "DISECT" are provided by the European Opendata Portal: CORDIS opendata.

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