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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.

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

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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