Opendata, web and dolomites

DiSect SIGNED

The Tumour Stroma as a Driver of Clonal Selection

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

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

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.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "DISECT" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.1.)

NanoPD_P (2020)

High throughput multiplexed trace-analyte screening for diagnostics applications

Read More  

Malaria POC (2019)

Ultrasensitive detection of transmissible malaria

Read More  

TOROS (2019)

A Theory-Oriented Real-Time Operating System for Temporally Sound Cyber-Physical Systems

Read More