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DNAmethAML SIGNED

Investigation of aberrant DNA methylation in malignant haematopoiesis

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 DNAmethAML project word cloud

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

advantage    seq    inhibitors    mark    degrees    myeloid    enhancer    enzyme    nature    dna    sequencing    mechanistic    throughput    hypermethylation    clinic    maintaining    somatic    transcriptional    inhibit    improvement    haematopoietic    alterations    altered    regulators    cancer    demethylation    tet2    atac    epigenetic    reversible    link    renewal    perform    therapies    patterns    mechanisms    genome    stem    malignancies    lost    crispr    blood    binding    suppressive    aberrant    mutated    acute    methyltransferase    secondly    sensitive    cell    aggressive    aml    promotes    clinically    sites    leads    regions    catalysing    enhancers    chip    annotate    uncontrollable    therapeutic    cells    plan    tumour    self    deficiency    transcription    distal    models    landscape    mouse    regulatory    methylc    combine    function    positive    leukaemia    mutations    frequently    diverse    screen    immature    varying    discovery    leukemic    leukaemogenesis    methylation    firstly   

Project "DNAmethAML" data sheet

The following table provides information about the project.

Coordinator
KOBENHAVNS UNIVERSITET 

Organization address
address: NORREGADE 10
city: KOBENHAVN
postcode: 1165
website: www.ku.dk

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 Denmark [DK]
 Total cost 200˙194 €
 EC max contribution 200˙194 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-01-01   to  2019-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KOBENHAVNS UNIVERSITET DK (KOBENHAVN) coordinator 200˙194.00

Map

 Project objective

Acute myeloid leukaemia (AML) is an aggressive type of blood cancer characterized by uncontrollable growth of immature myeloid cells. Somatic mutations in diverse transcriptional regulators result in aberrant epigenetic landscape in leukemic cells, including patterns of DNA methylation. Due to its reversible nature, this epigenetic mark has been a promising therapeutic target and DNA methyltransferase inhibitors are already being used with varying degrees of success in clinic. The targeted improvement of existing therapies requires a better understanding of mechanisms how altered DNA methylation promotes malignancies. TET2, an enzyme catalysing DNA demethylation, is one of the most frequently mutated epigenetic regulators in AML. Its loss leads to hypermethylation at distal regulatory regions (or enhancers) and increased stem cell self-renewal and leukaemogenesis in the haematopoietic system. In the proposed work I plan to investigate the link between aberrant hypermethylation at enhancers and its role in developing and maintaining AML. Firstly, I will take advantage of clinically relevant AML mouse models that combine TET2 deficiency with AML-specific alterations and annotate DNA methylation-sensitive enhancers using high-throughput sequencing methods (MethylC-seq, ATAC-seq and ChIP-seq). Secondly, I will perform a positive-selection CRISPR-based high-throughput enhancer screen to identify DNA methylation-sensitive enhancers that inhibit leukemic stem cell self-renewal (i.e. tumour suppressive regulatory regions). Finally, I will identify and study the function of transcription factors which binding is lost due to aberrant DNA hypermethylation at these sites. The proposed work will be both discovery-based (genome-wide level) as well as mechanistic.

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

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