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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 €

0

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.

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

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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