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PMLingAML SIGNED

Using PML nuclear body biology to identify potential AML treatment targets

Total Cost €

0

EC-Contrib. €

0

Partnership

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 PMLingAML project word cloud

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

therapy    npm1    nuclear    majority    body    stem    c65a    scrutinised    therapeutic    mouse    leukemogenesis    nb    strategies    trial    myeloid    previously    rar    successful    drug    vast    nbs    cells    mimics    cellular    underlying    relationship    mass    respective    spectrometry    models    murine    knock    roles    resolution    analysing    model    identification    outcome    mutation    damage    samples    decipher    acute    mechanisms    incl    formerly    patients    promyelocytes    npm1c    healthy    patient    treatment    leukemia    share    dynamics    mutated    progenitor    hematopoietic    localisation    pmlingaml    pmlc62a    biology    flt3itd    alpha    oncoprotein    poor    understanding    clinical    dna    lethal    carry    functions    repair    aml    isolated    pathogenesis    status    inter    imaging    leukemic    ber    cured    bone    lsk    marrows    dactinomycin    function    excision    combination    apl    assuredly    subset    elucidating    sumoylome    disrupted    base    shown    pml    disruption    initiation    promyelocytic   

Project "PMLingAML" 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 184˙707 €
 EC max contribution 184˙707 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-09-01   to  2022-08-31

 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 184˙707.00

Map

 Project objective

Understanding the initiation and development of acute myeloid leukemia (AML) represents an important challenge which may lead to the identification of new therapeutic strategies. Acute promyelocytic leukemia (APL) was formerly the most lethal subset of AML; however, today the vast majority of APL patients can be cured by combination therapy. Therefore, fully understanding the mechanisms underlying successful treatment, by analysing the biology of APL pathogenesis will assuredly improve the management of AML subsets associated with a poor outcome, such as NPM1-mutated AML. Using a novel knock-in mouse model, PmlC62A/C65A, which mimics Pml nuclear body (NB) disruption induced by the main oncoprotein PML-RARα in APL, we have previously shown that Pml NBs are essential in APL pathogenesis and treatment response. Our project “PMLingAML” aims to carry on elucidating the impact of Pml NB disruption in APL, and then to apply this knowledge in other AML subsets. To this end, a mass spectrometry analysis will be conducted on both hematopoietic stem and progenitor (LSK) cells and promyelocytes isolated from healthy and leukemic murine bone marrows, to decipher the consequences of Pml NB disruption on the SUMOylome. Next, since PML NBs and NPM1 share common cellular functions and characteristics, we will analyse the inter-relationship between them; their localisation and dynamics will be assessed according to their respective status (disruption, mutation, knock-out), for example by high resolution imaging, both in various healthy and leukemic mouse models (incl NPM1c and NPM1c/FLT3ITD), and in patient samples. Their respective roles in response to a drug under clinical trial, Dactinomycin, will also be scrutinised. Finally, as DNA damage repair is an important function disrupted during leukemogenesis, the roles of Pml NBs and Npm1 will be assessed together with their inter-relationship, with particular focus on the base excision repair (BER) pathway.

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