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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.

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

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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