Opendata, web and dolomites

ApoptoMDS SIGNED

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

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 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.

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

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.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "APOPTOMDS" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.1.)

ERC VP CSA (2018)

Support to the Vice-Presidents of the ERC Scientific Council 2018

Read More  

CELPRED (2020)

Circuit elements of the cortical circuit for predictive processing

Read More  

CohoSing (2019)

Cohomology and Singularities

Read More