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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.

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

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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