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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.

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

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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