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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.

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

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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