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AltCheM SIGNED

In vivo functional screens to decipher mechanisms of stochastically- and mutationally-induced chemoresistance in Acute Myeloid Leukemia

Total Cost €

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EC-Contrib. €

0

Partnership

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 AltCheM project word cloud

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

resistance    mutational    few    myeloid    predict    mutant    virtue    leukemia    collection    stochastically    despite    pooled    actively    model    firmly    treatment    poorly    decipher    effectors    decades    rna    screening    intrinsically    screen    molecular    chemoresistant    examined    minimal    aml    chemotherapy    reading    functional    profiling    predetermined    mice    genesis    modes    agents    experiments    frame    therapy    remission    combining    consequence    stochastic    mutations    chemoprotective    resistant    paradigm    regardless    chemoresistance    fraction    chemotherapeutic    resist    initial    hematology    mechanisms    shrna    vivo    persistence    residual    almost    biological    relevance    autonomous    cells    patients    characterization    mrd    underlying    prone    rounds    initiating    front    chip    innovative    status    diagnosed    fundamental    exome    pursue    standard    ultimately    expansion    sustained    relapse    survive    mutationally    genetically    sequencing    adults    therapies    consecutive    genomic    tested    re    conduct    acute    mll    emergence    mouse    cell    disease    libraries    combinations    af9    line   

Project "AltCheM" data sheet

The following table provides information about the project.

Coordinator
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE 

Organization address
address: RUE DE TOLBIAC 101
city: PARIS
postcode: 75654
website: www.inserm.fr

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 France [FR]
 Total cost 1˙500˙000 €
 EC max contribution 1˙500˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-STG
 Funding Scheme ERC-STG
 Starting year 2018
 Duration (year-month-day) from 2018-03-01   to  2023-02-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) coordinator 1˙500˙000.00

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 Project objective

Acute Myeloid Leukemia (AML), the most common leukemia diagnosed in adults, represents the paradigm of resistance to front-line therapies in hematology. Indeed, AML is so genetically complex that only few targeted therapies are currently tested in this disease and chemotherapy remains the only standard treatment for AML since the past four decades. Despite an initial sustained remission achieved by chemotherapeutic agents, almost all patients relapse with a chemoresistant minimal residual disease (MRD). The goal of my proposal is to characterize the still poorly understood biological mechanisms underlying persistence and emergence of MRD. MRD is the consequence of the re-expansion of leukemia-initiating cells that are intrinsically more resistant to chemotherapy. This cell fraction may be stochastically more prone to survive front-line therapy regardless of their mutational status (the stochastic model), or genetically predetermined to resist by virtue of a collection of chemoprotective mutations (the mutational model). I have already generated in mice, by consecutive rounds of chemotherapy, a stochastic MLL-AF9-driven chemoresistance model that I examined by RNA-sequencing. I will pursue the comprehensive cell autonomous and cell non-autonomous characterization of this chemoresistant AML disease using whole-exome and ChIP-sequencing. To establish a mutationally-induced chemoresistant mouse model, I will conduct an innovative in vivo screen using pooled mutant open reading frame and shRNA libraries in order to predict which combinations of mutations, among those already known in AML, actively promote chemoresistance. Finally, by combining genomic profiling and in vivo shRNA screening experiments, I will decipher the molecular mechanisms and identify the functional effectors of these two modes of resistance. Ultimately, I will then be able to firmly establish the fundamental relevance of the stochastic and/or the mutational model of chemoresistance for MRD genesis.

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

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