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ApoptoMDS SIGNED

Hematopoietic stem cell Apoptosis in bone marrow failure and MyeloDysplastic Syndromes: Friend or foe?

Total Cost €

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EC-Contrib. €

0

Partnership

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 ApoptoMDS project word cloud

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

mechanism    transplanted    pressure    hspc    engineered    mice    leukemia    delays    progression    correlate    bone    expand    kinetics    signaling    function    malignant    apoptosis    activated    acute    dna    marrow    dilemma    hematological    progenitor    syndrome    deregulation    tested    players    mds    phenotype    inactivate    serially    selective    undergoing    sufficient    severe    pave    symptomatic    susceptible    validated    congenital    overcome    hypersusceptibility    genetically    mitigates    symptoms    little    mouse    myelodysplastic    cells    xenotransplanted    samples    susceptibility    stage    syndromes    apoptomds    disadvantage    confers    stem    hypothesized    disease    evolution    turns    hematopoietic    risk    inhibiting    damage    draw    resistance    influences    myeloid    transformation    therapeutic    activation    checkpoint    patient    functional    patients    abrogation    period    competitive    aml    models    selects    collection    apoptotic    analyze    levels    pathogenesis    phenotypes    regulators    hspcs    contributes    deregulated   

Project "ApoptoMDS" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITAETSKLINIKUM FREIBURG 

Organization address
address: HUGSTETTER STRASSE 49
city: FREIBURG
postcode: 79106
website: n.a.

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 Germany [DE]
 Project website https://www.uniklinik-freiburg.de/index.php
 Total cost 1˙372˙525 €
 EC max contribution 1˙372˙525 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2014-STG
 Funding Scheme ERC-STG
 Starting year 2015
 Duration (year-month-day) from 2015-06-01   to  2020-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAETSKLINIKUM FREIBURG DE (FREIBURG) coordinator 1˙372˙525.00

Map

 Project objective

Deregulated apoptotic signaling in hematopoietic stem and progenitor cells (HSPCs) strongly contributes to the pathogenesis and phenotypes of congenital bone marrow failure and myelodysplastic syndromes (MDS) and their progression to acute myeloid leukemia (AML). HSPCs are highly susceptible to apoptosis during bone marrow failure and early MDS, but AML evolution selects for apoptosis resistance. Little is known about the main apoptotic players and their regulators. ApoptoMDS will investigate the impact of apoptotic deregulation for pathogenesis, correlate apoptotic susceptibility with the kinetics of disease progression and characterize the mechanism by which apoptotic susceptibility turns into resistance. ApoptoMDS will draw on a large collection of patient-derived samples and genetically engineered mouse models to investigate disease progression in serially transplanted and xenotransplanted mice. How activated DNA damage checkpoint signaling contributes to syndrome phenotypes and HSPC hypersusceptibility to apoptosis will be assessed. Checkpoint activation confers a competitive disadvantage, and HSPCs undergoing malignant transformation are under high selective pressure to inactivate it. Checkpoint abrogation mitigates the hematological phenotype, but increases the risk of AML evolution. ApoptoMDS aims to analyze if inhibiting apoptosis in HSPCs from bone marrow failure and early-stage MDS can overcome the dilemma of checkpoint abrogation. Whether inhibiting apoptosis is sufficient to improve HSPC function will be tested on several levels and validated in patient-derived samples. How inhibiting apoptosis in the presence of functional checkpoint signaling influences malignant transformation kinetics will be assessed. If, as hypothesized, inhibiting apoptosis both mitigates hematological symptoms and delays AML evolution, ApoptoMDS will pave the way for novel therapeutic approaches to expand the less severe symptomatic period for patients with these syndromes.

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

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