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GlioTarget SIGNED

Inflaming the microenvironment of glioblastoma tumors by ADAR1 inhibition: a two-hit approach for the treatment of brain cancer.

Total Cost €

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EC-Contrib. €

0

Partnership

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 GlioTarget project word cloud

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

therapies    isg    alone    cells    body    acting    fail    pharmacologic    primary    innate    vital    therapy    models    understand    patients    dsrnas    inhibit    stimulated    memories    sensitivity    survival    months    glioblastomas    outcomes    inhibition    inflammation    immune    date    orchestrate    endogenous    aberrant    tumor    clinical    care    trigger    combine    invariably    representing    interferon    functions    gbs    organ    cell    sensing    leads    mouse    adar1    cancer    hinder    human    immunotherapies    functionally    form    nature    checkpoint    immuno    heterogeneity    adenosine    tumors    gb    precious    emerged    therapeutic    self    oncology    standard    tme    infiltration    nucleic    14    newly    experiences    extreme    ultimately    stores    despite    deaminase    perform    genetic    isgs    supporting    simultaneously    molecular    edits    disrupt    central    lines    lethal    interactions    combination    otherwise    disheartening    diagnosed    brain    foreign    vulnerability    rna    core    individuals    microenvironment    arrest    malignancies    patient    acids    genes    social    immunity    immunosuppressive    15    pointing    frequent    expression    median    expressing   

Project "GlioTarget" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE DE LAUSANNE 

Organization address
address: Quartier Unil-Centre Bâtiment Unicentre
city: LAUSANNE
postcode: 1015
website: www.unil.ch

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 Switzerland [CH]
 Total cost 191˙149 €
 EC max contribution 191˙149 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2021
 Duration (year-month-day) from 2021-09-01   to  2023-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE LAUSANNE CH (LAUSANNE) coordinator 191˙149.00

Map

 Project objective

The brain is our most precious organ. Not only does it orchestrate vital body functions but it also stores memories and experiences, ultimately defining the core of our human nature. Brain malignancies are particularly disheartening because they disrupt our ability to perform as individuals and hinder our social interactions. Glioblastomas (GBs) represent the most frequent and lethal form of primary brain tumors, with a median survival of 14.6 months and 15,000 newly diagnosed patients per year in Europe and the US. Current therapies invariably fail, likely due to the extreme genetic heterogeneity of GB and the presence of a highly immunosuppressive tumor microenvironment (TME). Here, I propose to exploit an innate immunity checkpoint to simultaneously target cancer cells and their supporting TME. Adenosine Deaminase Acting on RNA 1 (ADAR1) is a central component of the RNA sensing pathway. It edits endogenous self dsRNAs, which would otherwise be recognized as foreign and trigger an aberrant innate immune response. Sensing of foreign nucleic acids results in interferon production which leads to cell-growth arrest, inflammation and immune cell infiltration through the expression of interferon-stimulated genes (ISGs). ADAR1 has recently emerged as a promising immuno-oncology target, with evidence pointing towards ADAR1 loss representing a novel vulnerability of ISG-expressing cancer cells. Despite expressing ISGs, GB tumors have not been evaluated for sensitivity to ADAR1 inhibition to date. I will therefore combine genetic and pharmacologic approaches to inhibit ADAR1 in patient-derived cancer cell lines and pre-clinical mouse models of GB. My aims are: i) to understand the molecular outcomes of ADAR1 inhibition in GB cancer cells; ii) to functionally characterize the TME of GBs upon ADAR1 inhibition; iii) to evaluate the therapeutic potential of ADAR1 inhibition alone and in combination with standard of care therapy and TME-targeted immunotherapies.

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

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