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CrIC SIGNED

Molecular basis of the cross-talk between chronic inflammation and cancer

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

CrIC project word cloud

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

fa spontaneous besides slx4 heightened cri proteins patients suppresses fanconi pathological virus accumulation transcripts inflammatory promotes absence syndrome immune deficiency dna model hallmark demonstrated degradation relationship damage endogenous binds revealing bone opening progressive thereby unveil nucleic hypothesis perspectives acids ing repression marrow unforeseen allelic mutations molecular pro levels cancer hiv dependent observation susceptibility immunodeficiency underlying defects bi cytokine treatment anemia reverse inflammation innate repair human severe onset

Project "CrIC" 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]
Total cost	1˙500˙000 €
EC max contribution	1˙500˙000 € (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 2015-04-01 to 2021-03-31

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS 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.	FR (PARIS)	coordinator	1˙500˙000.00

Map

Project objective

Cancer related inflammation (CRI) is a well-established hallmark of cancer. We recently demonstrated that the DNA damage repair SLX4 complex suppresses spontaneous and human immunodeficiency virus (HIV)-dependent pro-inflammatory cytokine production, revealing a role for this DNA repair complex in controlling innate immune responses. Bi-allelic mutations in SLX4 are involved in the onset of Fanconi Anemia (FA), a syndrome characterized, besides heightened cancer susceptibility, by severe defects of the immune system, resulting from increased pro-inflammatory cytokine levels and progressive bone marrow failure. Within this proposal, using SLX4-deficiency as a working model, I aim at investigating the molecular process underlying CRI. Based on our previous observation that the SLX4 complex binds to HIV-derived reverse-transcripts and promotes their degradation, my working hypothesis is that CRI results from the accumulation of endogenous pathological nucleic acids that are recognized by the innate immune system in the absence of SLX4. The present project should unveil the relationship between repression of pro-inflammatory cytokine production by proteins involved in DNA repair, DNA damage, and CRI, thereby opening unforeseen perspectives in the treatment of cancer patients.

Publications

List of publications.
year	authors and title	journal	last update
2016	Christelle BrÃ©gnard, Jessica Guerra, StÃ©phanie DÃ©jardin, Frank Passalacqua, Monsef Benkirane, Nadine Laguette Upregulated LINE-1 Activity in the Fanconi Anemia Cancer Susceptibility Syndrome Leads to Spontaneous Pro-inflammatory Cytokine Production published pages: 184-194, ISSN: 2352-3964, DOI: 10.1016/j.ebiom.2016.05.005	EBioMedicine 8	2020-01-24

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