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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.

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

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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