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Investigation of aberrant DNA methylation in malignant haematopoiesis

Total Cost €


EC-Contrib. €






 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.

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

Project "DNAmethAML" data sheet

The following table provides information about the project.


Organization address
address: NORREGADE 10
postcode: 1165

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


Take a look of project's partnership.

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


 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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