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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.

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

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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