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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.

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

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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