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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.

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

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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