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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.

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

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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