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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.

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

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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