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EVI1inCancer SIGNED

Overcoming the epigenetic and therapeutic barrier of EVI1-overexpressing cancers

Total Cost €

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EC-Contrib. €

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Partnership

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 EVI1inCancer project word cloud

Explore the words cloud of the EVI1inCancer project. It provides you a very rough idea of what is the project "EVI1inCancer" about.

therapy    interference    leukemia    ovarian    gata2    inhibition    sequences    master    vivo    genome    stemness    poorly    enhancer    small    reader    breakpoint    bet    sarcoma    decades    transcription    epigenetic    domain    aml    regulatory    profiling    experimental    tumors    mechanisms    chromatin    thereby    transformed    category    cell    colon    model    breast       goals    myeloid    therapies    reveal    superloading    amenable    solid    inhibitors    resistance    expressing    evi1    landscape    pressing    event    brd4    identification    retroelements    functional    specificity    editing    seek    deregulating    genetic    proteomic    experiments    therapeutic    lung    consequent    systematic    protein    genes    regulator    underlying    oncogene    components    prominently    establishes    relative    bromodomain    transforming    regulating    found    cancer    mechanism    tissue    rearranged    risk    genomic    acute    interactions    3q    pave    transpos    soft    lack    medical    characterization    inv    malignancies    function    deregulation    genomics   

Project "EVI1inCancer" data sheet

The following table provides information about the project.

Coordinator
DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG 

Organization address
address: IM NEUENHEIMER FELD 280
city: HEIDELBERG
postcode: 69120
website: www.dkfz.de

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 Germany [DE]
 Total cost 1˙499˙094 €
 EC max contribution 1˙499˙094 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-STG
 Funding Scheme ERC-STG
 Starting year 2016
 Duration (year-month-day) from 2016-06-01   to  2021-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG DE (HEIDELBERG) coordinator 1˙499˙094.00

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 Project objective

Deregulation of the EVI1 oncogene is a key transforming event in the development of many malignancies, most prominently very high-risk acute myeloid leukemia (AML), ovarian, colon, breast, non-small cell lung cancer, and soft-tissue sarcoma. For decades, both EVI1 function and the mechanism underlying its deregulation have been poorly understood. The consequent lack of a targeted therapy against EVI1 establishes a pressing medical need. In a recent study investigating a distinct category of EVI1-driven AML with inv(3) or t(3;3), we characterized the regulatory domain of EVI1 and identified a master regulatory element of the stemness factor GATA2 to be rearranged to EVI1, thereby deregulating both genes. Applying functional genomics and genome-editing, we found that the rearranged enhancer element adopted novel features, such as superloading of the epigenetic reader and chromatin regulator BRD4, allowing its inhibition with BET/bromodomain inhibitors with relative EVI1 specificity. Interference with EVI1-regulatory mechanisms thus has potential therapeutic value in EVI1-transformed tumors. To pave the way for epigenetic targeting of other EVI1-expressing malignancies, we aim to identify genomic enhancer sequences and protein components of the EVI1 regulatory domain by systematic epigenetic and proteomic profiling. Specifically, we seek to achieve the following experimental goals: (1) Identification of the mechanism underlying EVI1 deregulation in non-3q-rearranged AML and solid tumors; (2) Addressing the role of breakpoint-associated transpos-able retroelements; (3) Characterization of the transcription factor complex regulating EVI1; (4) Identification of epigenetic resistance mechanisms in EVI1 AML by using an in vivo model and a genome-editing approach. The proposed experiments will provide insight into the epigenetic landscape of EVI1 malignancies and help reveal new targets and genetic interactions amenable to future therapies in these high-risk malignancies.

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