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.

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

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.)

NanoPD_P (2020)

High throughput multiplexed trace-analyte screening for diagnostics applications

Read More  

Malaria POC (2019)

Ultrasensitive detection of transmissible malaria

Read More  

HyperBio (2019)

Vis-NIR Hyperspectral imaging for biomaterial quality control

Read More