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EpiTALL SIGNED

Dynamic interplay between DNA methylation, histone modifications and super enhancer activity in normal T cells and during malignant T cell transformation

Total Cost €

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EC-Contrib. €

0

Partnership

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 EpiTALL project word cloud

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

therapy    entity    adult    relapse    context    etps    aggressive    disease    transcriptional    chromatin    prognosis    oncogenes    subtypes    ultimate    intervention    lymphoblastic    histone    etp    treatment    die    programs    alls    originally    cell    15    regulation    progenitors    haematological    cells    drives    accounts    unravelled    refractory    yield    subset    humane    interplay    tumor    signature    patients    stem    basis    differentiation    pediatric    human    20    gene    extremely    precursors    genetic    poor    genome    dna    tackling    completely    architecture    methylation    expression    elucidating    chemotherapy    efforts    conceptual    dynamic    leukemia    survival    prognostic    improvements    serves    understand    ultimately    framework    markedly    suggests    acute    structure    50    patterns    critical    malignant    25    landscape    fail    malignancy    gradual    myeloid    oncogenic    epigenomic    hematopoietic    resemble    intensified    normal    failed    therapeutic    modifications    cancer    genetics    defines    precision   

Project "EpiTALL" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITEIT GENT 

Organization address
address: SINT PIETERSNIEUWSTRAAT 25
city: GENT
postcode: 9000
website: http://www.ugent.be

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 Belgium [BE]
 Total cost 958˙750 €
 EC max contribution 958˙750 € (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 2015-07-01   to  2020-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITEIT GENT BE (GENT) coordinator 958˙750.00

Map

 Project objective

Dynamic interplay between histone modifications and DNA methylation defines the chromatin structure of the humane genome and serves as a conceptual framework to understand transcriptional regulation in normal development and human disease. The ultimate goal of this research proposal is to study the chromatin architecture during normal and malignant T cell differentiation in order to define how DNA methylation drives oncogenic gene expression as a novel concept in cancer research.

T-cell acute lymphoblastic leukemia (T-ALL) accounts for 15% of pediatric and 25% of adult ALL cases and was originally identified as a highly aggressive tumor entity. T-ALL therapy has been intensified leading to gradual improvements in survival. However, 20% of pediatric and 50% of adult T-ALL cases still relapse and ultimately die because of refractory disease. Research efforts have unravelled the complex genetic basis of T-ALL but failed to identify new promising targets for precision therapy.

Recent studies have identified a subset of T-ALLs whose transcriptional programs resemble those of early T-cell progenitors (ETPs), myeloid precursors and hematopoietic stem cells. Importantly, these so-called ETP-ALLs are characterized by early treatment failure and an extremely poor prognosis. The unique ETP-ALL gene expression signature suggests that the epigenomic landscape in ETP-ALL is markedly different as compared to other genetic subtypes of human T-ALL.

My project aims to identify genome-wide patterns of DNA methylation and histone modifications in genetic subtypes of human T-ALL as a basis for elucidating how DNA methylation drives the expression of critical oncogenes in the context of poor prognostic ETP-ALL. Given that these ETP-ALL patients completely fail current chemotherapy treatment, tackling this completely novel aspect of ETP-ALL genetics will yield new targets for therapeutic intervention in this aggressive haematological malignancy.

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

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