Opendata, web and dolomites

altEJrepair SIGNED

Characterisation of DNA Double-Strand Break Repair by Alternative End-Joining: Potential Targets for Cancer Therapy

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 altEJrepair project word cloud

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

effectiveness    shedding    treatment    dna    small    anticancer    absence    damage    progression    history    cell    molecular    tumour    few    alt    last    signature    elusive    elucidating    remission    integral    recognition    paving    hr    mediated    multidisciplinary    theta    basic    joining    identification    polymerase    homologous    therapeutics    gaining    viability    molecule    resolves    implications    network    hrd    pol    chemotherapeutics    intricate    regulated    light    repair    mechanisms    additionally    lesions    genetic    crosstalk    deficient    shown    contributes    contribution    tumours    despite    clinical    recombination    players    changing    interconnections    regulation    inhibitors    interplay    characterise    convinced    humans    senses    action    alternative    drug    treatments    function    preventing    cancer    patients    lethality    poorly    survival    elucidate    abovementioned    minimise    critical    relevance    synthetic    pathogenic    mutational    composition    ej    utilisation    limited    characterised   

Project "altEJrepair" data sheet

The following table provides information about the project.

Coordinator
INSTITUT CURIE 

Organization address
address: rue d'Ulm 26
city: PARIS
postcode: 75231
website: www.curie.fr

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 France [FR]
 Total cost 1˙498˙750 €
 EC max contribution 1˙498˙750 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2016-STG
 Funding Scheme ERC-STG
 Starting year 2017
 Duration (year-month-day) from 2017-07-01   to  2022-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT CURIE FR (PARIS) coordinator 1˙498˙750.00

Map

 Project objective

DNA repair pathways evolved as an intricate network that senses DNA damage and resolves it in order to minimise genetic lesions and thus preventing tumour formation. Gaining in recognition the last few years, the alternative end-joining (alt-EJ) DNA repair pathway was recently shown to be up-regulated and required for cancer cell viability in the absence of homologous recombination-mediated repair (HR). Despite this integral role, the alt-EJ repair pathway remains poorly characterised in humans. As such, its molecular composition, regulation and crosstalk with HR and other repair pathways remain elusive. Additionally, the contribution of the alt-EJ pathway to tumour progression as well as the identification of a mutational signature associated with the use of alt-EJ has not yet been investigated. Moreover, the clinical relevance of developing small-molecule inhibitors targeting players in the alt-EJ pathway, such as the polymerase Pol Theta (Polθ), is of importance as current anticancer drug treatments have shown limited effectiveness in achieving cancer remission in patients with HR-deficient (HRD) tumours.

Here, we propose a novel, multidisciplinary approach that aims to characterise the players and mechanisms of action involved in the utilisation of alt-EJ in cancer. This understanding will better elucidate the changing interplay between different DNA repair pathways, thus shedding light on whether and how the use of alt-EJ contributes to the pathogenic history and survival of HRD tumours, eventually paving the way for the development of novel anticancer therapeutics.

For all the abovementioned reasons, we are convinced this project will have important implications in: 1) elucidating critical interconnections between DNA repair pathways, 2) improving the basic understanding of the composition, regulation and function of the alt-EJ pathway, and 3) facilitating the development of new synthetic lethality-based chemotherapeutics for the treatment of HRD tumours.

 Publications

year authors and title journal last update
List of publications.
2016 Zeina Kais, Beatrice Rondinelli, Amie Holmes, Colin O’Leary, David Kozono, Alan D. D’Andrea, Raphael Ceccaldi
FANCD2 Maintains Fork Stability in BRCA1/2-Deficient Tumors and Promotes Alternative End-Joining DNA Repair
published pages: 2488-2499, ISSN: 2211-1247, DOI: 10.1016/j.celrep.2016.05.031
Cell Reports 15/11 2020-03-25

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "ALTEJREPAIR" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.1.)

ZARAH (2020)

Women’s labour activism in Eastern Europe and transnationally, from the age of empires to the late 20th century

Read More  

SWIP (2019)

Extended short-wave infrared pulsed fibre laser

Read More  

MOCHA (2019)

Understanding and leveraging ‘moments of change’ for pro-environmental behaviour shifts

Read More