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DREMATURE SIGNED

DNA repair mechanisms and therapy resistance of BRCA2-deficient cancers

Total Cost €

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EC-Contrib. €

0

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.

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

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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