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FAtoUnFRAGILITY SIGNED

Fanconi anemia : a disease model to understand causes and consequences of common fragile site instability.

Total Cost €

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EC-Contrib. €

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Partnership

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Project "FAtoUnFRAGILITY" data sheet

The following table provides information about the project.

Coordinator
CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS 

Organization address
address: RUE MICHEL ANGE 3
city: PARIS
postcode: 75794
website: www.cnrs.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]
 Project website https://www.gustaveroussy.fr/en/stress-replicatif-instabilite-genetique-et-mitose-thematique
 Total cost 1˙462˙383 €
 EC max contribution 1˙462˙383 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2014-STG
 Funding Scheme ERC-STG
 Starting year 2015
 Duration (year-month-day) from 2015-06-01   to  2020-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS FR (PARIS) coordinator 1˙462˙383.00

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 Project objective

Originally described by cytogeneticists, common fragile sites (CFSs) are chromosomal regions known for their susceptibility to break and rearrange aberrantly, thus altering the expression of genes located therein. CFS instability is associated with tumor development and pathogenic copy number variations. Recent advances have significantly contributed to dissect the molecular bases of CFS instability, yet a unifying model for their unique breakage propensity has not been determined. Fanconi anemia (FA) is a chromosomal instability syndrome featuring congenital abnormalities, bone marrow failure and cancer predisposition, characterized by an increased CFS fragility. FA is thus an ideal model to understand the mechanisms underpinning CFS instability and the mechanistic link between CFS instability and the pathogenesis of disease phenotypes. I propose to use FA cellular models to examine the molecular events leading to CFS instability, and FA mouse models to investigate the consequences of deletions, amplifications or rearrangements involving CFSs on the expression of genes regulating critical signal transduction pathways involved in cell survival, proliferation, and differentiation. Exploring these mechanisms can lead to the development of chemopreventive or therapeutic strategies targeting aberrant gene expression or pathological pathways.

 Publications

year authors and title journal last update
List of publications.
2019 Philippe Fernandes, Benoit Miotto, Claude Saint-Ruf, Viola Nähse, Silvia Ravera, Enrico Cappelli, Valeria Naim
FANCD2 tunes the UPR preventing mitochondrial stress--induced common fragile site instability
published pages: , ISSN: , DOI: 10.1101/808915
2019-12-16
2019 Michalis Fragkos, Viviana Barra, Tom Egger, Benoit Bordignon, Delphine Lemacon, Valeria Naim and Arnaud Coquelle
Dicer prevents genome instability in response to replication stress
published pages: , ISSN: 1949-2553, DOI: 10.18632/oncotarget.27034
Oncotarget 10/43 2019-12-16
2017 Michalis Fragkos, Valeria Naim
Rescue from replication stress during mitosis
published pages: 1-21, ISSN: 1538-4101, DOI: 10.1080/15384101.2017.1288322
Cell Cycle 2019-05-29

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