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Overcoming the epigenetic and therapeutic barrier of EVI1-overexpressing cancers

Total Cost €


EC-Contrib. €






 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.

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

Project "EVI1inCancer" data sheet

The following table provides information about the project.


Organization address
postcode: 69120

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


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 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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