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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.

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

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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