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INTUMORX

Elucidation of intratumoral heterogeneity in Kras-driven cancers

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 INTUMORX project word cloud

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

tracing    mouse    maintenance    crispr    molecular    tissues    molecules    indicate    propagation    suppressed    cancer    cellular    vivo    vitro    cancers    variability    tumor    regeneration    experiments    therapy    lineage    hierarchical    considerable    phenotypes    lentiviral    molecule    model    selective    mice    adenocarcinomas    tumors    elucidate    reporter    resistant    intratumoral    responder    subpopulation    context    cellullar    modified    vectors    forming    signaling    provides    silencing    multiclonality    tissue    cells    survival    signal    stasis    efforts    leads    microenvironments    prolonged    luad    krasg12d    populations    reconstitution    epithelial    human    delta    ed    population    therapeutic    tp53    components    wnt    had    engineered    strikingly    probablility    signals    treatment    combination    genetically    inhibitors    normal    stem    heterogeneity    collectively    small    exhibited    hypothesized    demonstrated    ablation    mechanisms    cell    resistance    niche    kp    advantageous    autochthonous    lung   

Project "INTUMORX" data sheet

The following table provides information about the project.

Coordinator
HELSINGIN YLIOPISTO 

Organization address
address: YLIOPISTONKATU 3
city: HELSINGIN YLIOPISTO
postcode: 14
website: www.helsinki.fi

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 Finland [FI]
 Total cost 1˙972˙905 €
 EC max contribution 1˙972˙905 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2016-STG
 Funding Scheme ERC-STG
 Starting year 2017
 Duration (year-month-day) from 2017-07-01   to  2022-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    HELSINGIN YLIOPISTO FI (HELSINGIN YLIOPISTO) coordinator 1˙972˙905.00

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 Project objective

The considerable variability within tissue microenvironments as well as the multiclonality of cancers leads to intratumoral heterogeneity. This increases the probablility of cellular states that promote resistance to therapy and eventually lead to reconstitution of the tumor by treatment-resistant cancer cells, which in some cases have properties of normal tissue stem cells. Wnt signals are important in the maintenance of stem cells in various epithelial tissues, including in lung development and regeneration. We hypothesized that Wnt signals contribute to tumor heterogeneity in genetically engineered KrasG12D; Tp53Δ/Δ (”KP”) mouse lung adenocarcinomas (LUAD). We observed that a subpopulation of LUAD cells exhibited high Wnt reporter activity and had increased tumor forming ability, which could be suppressed by silencing of Wnt signaling pathway components or by small molecule Wnt inhibitors in vitro and in vivo. KP LUAD cells show hierarchical features with two distinct populations, one with increased Wnt reporter activity and another forming a niche that provides the Wnt signal. Lineage-tracing experiments in the autochthonous KP tumors demonstrated that Wnt responder cells have increased tumor propagation ability in vivo. Strikingly, selective ablation of the Wnt responder cells resulted in tumor stasis. CRISPR-based targeting or small molecules targeting Wnt signaling reduced tumor growth and prolonged survival in the autochthonous KP mouse lung cancer model. These results indicate that maintenance of heterogeneity within tumors may be advantageous for the tumor cell population collectively. We propose to elucidate the molecular and cellullar mechanisms that control stem-like and niche cell phenotypes using a combination of novel lentiviral vectors and genetically modified mice in the context of the KP LUAD model. These efforts may lead to novel therapeutic concepts in human lung cancer.

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