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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.

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

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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