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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.

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

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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