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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.

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

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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