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DREMATURE SIGNED

DNA repair mechanisms and therapy resistance of BRCA2-deficient cancers

Total Cost €

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EC-Contrib. €

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Partnership

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 DREMATURE project word cloud

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

die    patient    image    engineered    genes    repair    innovative    strategies    normal    resistant    expertise    dna    homologous    mimics    lack    survive    largely    survival    existence    vitro    intact    candidates    biosensors    functional    cas9    jammed    oncology    genetically    ribose    occurs    strategy    escape    recombination    drug    damage    generation    cancer    mouse    breast    visualize    reduces    polymerase    candidate    combination    sophisticated    believe    overcome    resistance    lethality    model    modern    brca2    organoid    employ    smart    specificity    inhibitors    imaging    basic    crispr    interesting    driving    whereas    convinced    human    efficacy    am    spontaneous    decision    therapy    death    claspin    yielded    despite    deficient    synthetic    screens    molecular    cancers    3d    tumor    genetic    physiologically    poly    sequencing    cultures    disseminated    mechanisms    treatment    treatments    clinical    anti    alternative    rely    unknown    patients    mdc1    parpi    adp    cells    ovarian    synergizing    hr    start    defect    closely    tumors    function    disease    animals    dynamics    brca1    vivo   

Project "DREMATURE" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITAET BERN 

Organization address
address: HOCHSCHULSTRASSE 6
city: BERN
postcode: 3012
website: http://www.unibe.ch

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 Switzerland [CH]
 Total cost 187˙419 €
 EC max contribution 187˙419 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-01-01   to  2019-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAET BERN CH (BERN) coordinator 187˙419.00

Map

 Project objective

Despite the existence of various novel anti-cancer treatments, drug resistance remains a major cause of death in patients with disseminated cancer. To increase specificity and efficacy, modern treatment strategies in molecular oncology employ the “synthetic lethality” concept. An example are BRCA1/2-deficient breast and ovarian cancers that lack DNA repair by homologous recombination (HR). Due to this defect, tumor cells rely more on other DNA repair pathways. When such alternative pathways are jammed, e.g. by poly(ADP-ribose) polymerase inhibitors (PARPi), normal cells with intact HR can survive, whereas cancer cells die. However, even with this sophisticated treatment strategy, resistance to PARPi still occurs and greatly reduces patient survival. The mechanisms driving this resistance are still largely unknown. The main goal of this project is to advance the knowledge on therapy resistance by using a genetically engineered mouse model of BRCA2-deficient breast cancer, which closely mimics the human disease. Like in patients, cancer cells in these animals eventually escape from therapy. I will start by synergizing the next generation sequencing analysis of spontaneous resistant mouse tumors with functional genetic screens using the CRISPR/Cas9 technology. This combination has yielded interesting candidate genes whose loss of function may cause resistance. Two promising candidates, MDC1 and Claspin, will be further investigated using innovative and physiologically relevant 3D tumor organoid cultures. Moreover, I will apply my expertise in modern imaging technology to develop novel approaches to visualize DNA repair dynamics in resistant tumors in vitro and in vivo. I am convinced that by understanding basic resistance mechanisms, smart biosensors can be built to image the DNA damage response and eventually improve clinical decision making. I believe this project will have an impact on the design of strategies to overcome therapy escape in human cancer patients.

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The information about "DREMATURE" are provided by the European Opendata Portal: CORDIS opendata.

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