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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. €

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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.

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

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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