Data-Gouv-ML/pcri-actions-marie-curie-participations-et-projets-laureats huggingface dataset:
Projet GLIO-NET (Horizon Europe, appel à projets 2024)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Life Sciences
Statut du projet : SIGNED

Pediatric-type diffuse high-grade gliomas are the primary cause of cancer-related mortality in children and adolescents. The most common and aggressive forms harbor mutually exclusive mutations in histone 3 (H3), involving distinct brain regions and developmental origins. In contrast to other gliomas, GABAergic interneuron progenitors are implicated as the cells of origin for H3G34-mutant diffuse hemispheric gliomas (DHGs), which almost exclusively affect the cerebral hemispheres.  Seizures are a common comorbidity in patients with cortical gliomas, with evidence suggesting that gliomas alter synaptic structures to induce hyperexcitability. Neuronal activity, in turn, accelerates glioma progression through paracrine signaling and neuron-to-glioma synapses. Despite their cortical involvement, high seizure incidence, and poor prognosis, neuron-glioma interactions in DHGs remain understudied.  Human cerebral organoids, pioneered by the Knoblich Lab, recapitulate early brain architecture and circuit assembly via excitatory neurogenesis (dorsal forebrain) and interneuron development (ventral forebrain). Ultimately leading to functional network activity with complex oscillatory dynamics, organoids provide the ideal platform to study brain tumors in the context of network pathologies.  In this project, I will develop patient-derived models of seizure-associated DHGs in brain region specific cerebral organoids to examine neuron-glioma synapses. Using barcoded viral tracing and genetic perturbation screening, I will identify synaptic interaction partners and tumor-specific anti-connectivity targets. Electrophysiological recordings will assess the effects of anti-epileptogenic and anti-tumorigenic perturbations. This work will provide critical insights into neuron-glioma communication and its role in epileptogenesis during tumor progression, with important therapeutic implications.

Mots clés : brain organoids brain tumors pediatric glioma cancer neuronal connectivity neural networks synaptic tracing crispr screening epileptogenesis seizure activity epilepsy electrophysiology

Participants :
- Institut für Molekulare Biotechnologie (Autriche) — Coordinator, beneficiary, Organismes privés (hors enseignement), subvention : 230184.72 €
Projet LAMA2-TFIMG (Horizon Europe, appel à projets 2023)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Life Sciences
Statut du projet : SIGNED

Merosin-deficient congenital muscular dystrophy (LAMA2-RD) is caused by mutations in the LAMA2 gene, coding for the α2 subunit of laminin-211 (merosin). Typically, LAMA2-RD patients with absent merosin are clinically severe and unable to walk, while those producing a partially functional merosin are clinically milder. I identified a unique family in which the oldest of two affected siblings shows a novel and extremely mild phenotype despite the complete lack of merosin. This patient is still ambulant at 33 years with no respiratory insufficiency or cardiomyopathy. Notably, this patient carries the same LAMA2 loss-of-function mutation as the sibling who followed the typical severe disease course. Hypothesizing that genetic modifier(s) in the atypical patient mitigate the consequences of complete merosin deficiency via a novel mechanism, I isolated unique ultra-rare polymorphisms in genetic factors related to genes expressed in the atypical patient muscle but not in muscle of non-related LAMA2-RD patients, and I identified a novel candidate modifier controlling both fibrosis and inflammation (key drivers of LAMA2-RD pathogenesis). Given that this modifier is severely upregulated in the control LAMA2-RD patients but highly downregulated in the atypical patient, I will decrease its expression in the severely affected LAMA2-RD mouse model DyW/DyW by using the CRISPR-interference tool delivered by a single AAV9. I will then assess motor strength and endurance in treated mice. Finally, I will isolate highly affected muscles and sciatic nerve to characterize any molecular and morphological change occurring in these tissues upon modulating the modifier gene expression. I expect to observe functional improvement in LAMA2-RD animals, thus ameliorating their phenotype. The proposed project will elucidate novel mechanisms attenuating LAMA2-RD severity and will allow me to design new therapeutic approaches for this disorder for which, to date, there is no approved treatment.

Mots clés : muscular dystrophy, modifier genes, crispri, gene therapy, lama2 rd

Participants :
- Istituti di Ricovero e Cura a Carattere Scientifico (Italie) — Coordinator, beneficiary, Organismes privés (hors enseignement), subvention : 172750.08 €
Projet LIBRA (Horizon Europe, appel à projets 2023)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Economic Sciences
Statut du projet : SIGNED

LIBRA (Leveraging artificial Intelligence to Balance tRade-offs in the digital economy) will assess and compute positive and negative impacts on AI systems on society and the environment and it will optimize them to support policy-makers in Europe and beyond. Artificial Intelligence (AI) contributes to the development of the digital economy and expands the opportunities for sustainable development. However, as computing needs grow, AI systems and applications raise concerns about their environmental implications. Acknowledging this trade-off and achieving an optimal combination between the carbon footprint of AI systems and the benefits they contribute spurring is becoming a key policy concern, but remains an unresolved issue. By combining finance, AI and decision theory, LIBRA aims at filling this gap developing, testing and proposing policy-oriented innovative approaches and tools to: (i) map how investments in AI systems and applications contribute to generating carbon emissions worldwide; (ii) discover how the digital economy enables the achievement of the 17 Sustainable Development Goals (SDGs); (iii) compute the optimal balance between carbon emissions and sustainability objectives to inform national policies. LIBRA will contribute to the ongoing debate about AI and sustainability by combining approaches from computer science (i.e., Natural Language Processing and Deep Reinforcement Learning), complex systems (i.e., network science) and economics (i.e., decision theory) in a holistic framework. The project outcomes will support the discussion around the EU AI Act and the development of a solid sustainability roadmap which accounts for the growing opportunities spurred by the digital economy. LIBRA will last 24 months and it will be mainly conducted at the Royal Institute of Technology (KTH) in Stockholm (Sweden) with a secondment period at the University of Zurich (UZH) in Zurich (Switzerland).

Mots clés : digital economy sustainable development goals

Participants :
- KTH Institut royal de technologie (Suède) — Coordinator, beneficiary, Enseignement supérieur ou secondaire, subvention : 222727.68 €
- Université de Zurich (Suisse) — Partner, associated partner, Enseignement supérieur ou secondaire, subvention : 0.0 €
Projet immunoMet (Horizon Europe, appel à projets 2022)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Life Sciences
Statut du projet : SIGNED

Most cancer patients are resistant to immunotherapies, especially patients with liver and bone metastases. This suggests that during metastasis, cells acquire additional immune evasion mechanisms that dictate susceptibility to immunotherapies. Current immunotherapies initiate T cell-mediated killing of cancer cells. However, combining them with agents that target other immune cells in the body, such as natural killer (NK) cells, may be more effective. Whether immune evasion mechanisms of metastatic cells differ between organs and whether these mechanisms can be targeted to improve immunotherapeutic strategies remains unknown. The first aim of this proposal is to leverage a molecular barcoding technique named CaTCH (CRISPRa tracing of clones in heterogenous cell populations) to search for new mechanisms of NK cell immune evasion. CaTCH enables tracing metastatic cancer cells in vivo and isolating clones in a barcode-specific manner for subsequent characterization and functional experiments. We engineered a human non-small-cell lung cancer model with a complex CaTCH barcoding library. Subsequently, we injected the cells into mice harboring NK cells and mice having no NK cells in an experimental metastasis assay. We identified several barcoded clones enriched in specific organs under immune pressure. I aim to investigate this dataset to find novel mechanisms of NK cell immune evasion in the metastatic environment. In the second aim, I will combine molecular barcoding with replicative history tracing of cells to identify cancer clones that evade immune-mediated dormancy in the metastatic niche. I will compare the transcriptional and molecular profiles of dividing cells high in abundance to dividing cells low in abundance to find novel mediators of immune-mediated dormancy. The successful implementation of these aims will uncover new immune evasion strategies of metastatic cells that will pave the way for novel immunotherapeutic strategies for cancer patients.

Mots clés : metastasis, immune evasion, molecular barcoding, crispra

Participants :
- Research Institute of Molecular Pathology (Autriche) — Coordinator, beneficiary, Organismes privés (hors enseignement), subvention : 183600.96 €
Projet NetRewild (Horizon Europe, appel à projets 2024)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Environment and Geosciences
Statut du projet : SIGNED

Scaling up ecosystem restoration is critical during the UN Decade of Ecosystem Restoration (2021-2030) to combat the climate crisis, enhance biodiversity and restore essential ecosystem services. Trophic rewilding, which often involves the reintroduction of species to reinstate natural processes, is promising but remains controversial due to uncertainties about its broader, long-term impacts on ecosystems. To address these concerns, further research is needed to guide effective, science-based restoration efforts.  In this context, NetRewild addresses key challenges in restoration ecology by focusing on the complexity of species interaction networks that drive ecosystem processes. Interaction networks serve as a key link between individual species and overall ecosystem properties such as structure, stability, and function. This innovative approach moves beyond traditional restoration methods, which typically emphasize individual species or habitats, offering a more holistic perspective on ecosystem dynamics. NetRewild will use trait-based models to predict animal-plant interactions and associated ecological functions, such as seed dispersal and plant regeneration, based on species traits and assemblages across Natura 2000 sites. The research will focus on two main areas: first, how functional traits explain the mechanisms driving interaction patterns and ecological processes, addressing a critical knowledge gap essential for predicting future ecosystem impacts; second, how historical changes in herbivore communities and future rewilding scenarios shape ecosystem function and stability. The expected results will provide a science-based foundation for actionable strategies to support successful rewilding initiatives, while integrating insights from real-world applications.

Mots clés : ecological networks, restoration ecology, rewilding, species re introductions, megafauna, ecosystem stability, ecosystem function, predictive models, nature based solutions

Participants :
- Université d'Aarhus (Danemark) — Coordinator, beneficiary, Enseignement supérieur ou secondaire, subvention : 329241.6 €
- Stichting rewilding europe (Pays-Bas) — Partner, associated partner, Autres, subvention : 0.0 €
- Université de Zurich (Suisse) — Partner, associated partner, Enseignement supérieur ou secondaire, subvention : 0.0 €
Projet SITES (Horizon Europe, appel à projets 2022)
Action : Postdoctoral Fellowships - Global Fellowships
Panel : Physics
Statut du projet : SIGNED

A temporal Kerr cavity soliton (CS) is an optical pulse that propagates undistributed in a low-loss passive resonator. As part of its energy periodically escapes the resonator at each roundtrip, it forms a pulse train. Owing to their ultra-high stability compared to the pulses generated by mode-locked lasers, CSs are expected to play a crucial role in the future of atomic clocks, frequency combs, and high-precision metrology. Besides their inherent stability, they exhibit particle-like behavior. In particular, a couple of CSs can interact in the resonator and eventually form a bound state. Depending on the interaction, such coupled states can be more robust than the single-CS state itself. The aim of SITES (Solitons in time-multiplexed resonators) is to study, theoretically and experimentally, how temporal couplings within an optical resonator lead to the emergence of dynamic behaviors and cavity solitons that do not occur otherwise. On the applied side, SITES can give rise to a new kind of ultra-stable pulse train. On the fundamental front, SITES aims to investigate how these couplings between CSs can be leveraged for computational purposes and used to simulate specific crystal lattices. Such synthetic lattice combined with particle-like CSs leads to a fertile ground for the investigation of nonlinear effects in bosonic systems. Despite these strong fundamental and applied reasons, versatile couplings between multiple CSs have not been experimentally explored so far, mainly because the significant losses arising from the couplings prohibit reaching the intriguing nonlinear regimes. The experimental approach of SITES will overcome such a challenge and enables the realization of previously inaccessible coupled CSs.

Mots clés : cavity solitons, fiber optics, frequency combs, temporal couplings, synthetic lattice, coherent ising machine

Participants :
- Institut de technologie de Californie (Etats-Unis) — Partner, associated partner, Enseignement supérieur ou secondaire, subvention : 0.0 €
- Université libre de Bruxelles (Belgique) — Coordinator, beneficiary, Enseignement supérieur ou secondaire, subvention : 266684.16 €
Projet Beta_cell_protection (Horizon Europe, appel à projets 2024)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Life Sciences
Statut du projet : SIGNED

Type 1 Diabetes (T1D) is a chronic autoimmune disease characterized by the destruction of pancreatic β-cells, leading to insulin deficiency and severe complications, including cardiovascular disease, neuropathy, and vision impairment. Despite extensive research, the exact cause of T1D remains elusive, and the disease remains incurable. Emerging evidence suggests that β-cells may play an active role in their own demise, alongside the well-documented immune attack. Recent findings have identified protective genes within β-cells that may help them resist immune-mediated destruction. This project aims to investigate the role of three protective genes—HLA-E, IDO1, and BiP—in preserving β-cell function and survival under autoimmune stress. These genes were identified via a bioinformatic approach that analysed single cell RNA sequencing of β-cells from individuals affected by T1D. The study will begin by modulating the expression of these genes in human EndoC-βH1 cells and human islets, followed by an immune attack model of co-culture with the activated CD8+ T-cells. The goal is to determine which gene(s) offers the most significant protection against β-cell destruction. Subsequently, the most promising gene(s) will be further evaluated in stem cell-derived β-like cells, which will undergo in vivo testing in immune incompetent NSG mice to mimic more physiologically relevant conditions. The implanted cells will be evaluated by in vivo imaging using an intravital microscopy platform. By silencing or overexpressing these genes, we aim to elucidate the mechanisms that contribute to β-cell resilience, providing insights that could lead to novel therapeutic strategies for enhancing β-cell survival in T1D patients. This project represents a critical step forward in understanding the interplay between β-cells and the immune system in T1D. It has the potential to uncover new targets for therapy, ultimately improving the quality of life for individuals living with T1D.

Mots clés : cells, apoptosis, protective genes, cell homeostasis, type 1 diabetes, interferons

Participants :
- Université libre de Bruxelles (Belgique) — Coordinator, beneficiary, Enseignement supérieur ou secondaire, subvention : 200400.0 €
Projet PROSTarget (Horizon Europe, appel à projets 2022)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Life Sciences
Statut du projet : TERMINATED

Cancer cells dissemination from primary tumors to distant sites is the most terrifying evolving process of cancer. Such an irreversible and irreparable process encompasses tumor cells’ escaping, extravasating into blood stream and colonizing distant sites and is known as metastasis origin. Metastases spread is the leading cause of cancer-related deaths. The scattered but aggressive nature of metastatic disease and the extensive but not striking treatment effort history of metastatic cancers represents still a major obstacle in scientific progress and curability rates stemming from translational cancer research. Prostate cancer (PCa) hits men with high incidence and shows heterogeneity and resistance to standard of care. Altogether those hints imply that patients exhibiting disease progression, will head into complications succumbing to PCa-related high mortality, representing a major socio-economic problem world-wide. Importantly, PCa metastasis strikes after resistance acquisition to antiandrogens and taxols, overall limiting treatment efficacy. In this context, cancer research is vital with the aim of shedding new light on causal factors, unrevealing molecular mediators of the metastatic process, responsible for treatment resistance leading to patients’ poor overall survival. Finding those responsible mediators represents still an unmet medical need to reduce PCa mortality rate. Here we undertake an innovative translational approach to identify molecular cues underlying metastatic PCa. We focus our attention on a poorly characterized cancer entity: castration-naïve metastatic PCa , encompassing a tumor type that is metastatic at the time of first diagnosis. This tumor type is responsible for more than 50% of lethal PCa in the developed world. Through the project we will unleash prostate cancer vulnerabilities, to finally improve patient overall survival. For this reason, we built: PROSTarget

Mots clés : cancer progression, metastatic cascade, metastasis, dormancy, prostate cancer, molecular drivers, aggressive, patient survival, therapy resistance, drug discovery, metabolism, 

Participants :
- Institut de recherche en biomédecine (Espagne) — Coordinator, beneficiary, Recherche, subvention : 165312.96 €
- Université libre de Bruxelles (Belgique) — Partner, associated partner, Enseignement supérieur ou secondaire, subvention : 0.0 €
Projet DIVUNPKO (Horizon Europe, appel à projets 2024)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Social Sciences and Humanities
Statut du projet : SIGNED

Diversity in the United Nations Peacekeeping Bureaucracy (DIVUNPKO) addresses two critical issues. On the one hand, geographical diversity is a peculiarity of International Organizations’ staff like the United Nations (UN) and the European Union. Yet, in the literature, we have little knowledge about the impacts of staff diversity on the functioning of International Organizations (IOs). On the other hand, scholars have started to acknowledge the importance of diversity in peacekeeping operations but have studied it only for military staff. The present project fills these gaps by examining the impact of staff geographical diversity in the case of peacekeeping operations, the main tool of the UN for maintaining international peace and security. It adopts an interdisciplinary perspective by bridging diversity research in Public Administration and the literature on IOs and peacekeeping in International Relations. This two-year project has three objectives: (1) to collect socio-demographic data on civilian staff working in UN peacekeeping operations, 2) to develop an analytical framework to study diversity effects within IOs, and (3) to examine empirically the effects of geographical diversity among civilian peacekeepers along three dimensions: throughput, output and legitimacy. This project will make key contributions to the research on peacekeeping, international bureaucracies, and diversity. At the societal level, this project hopes to impact the work of international civilian missions and sensitize the public to issues of diversity in public organizations more broadly.

Mots clés : peacekeeping, diversity, united nations, international organizations

Participants :
- Fondation nationale des sciences politiques (France) — Coordinator, beneficiary, Enseignement supérieur ou secondaire, subvention : 242260.56 €
Projet Lithium-Ion Battery (Horizon Europe, appel à projets 2022)
Action : Postdoctoral Fellowships - European Fellowships
Panel : Information Science and Engineering
Statut du projet : SIGNED

Lithium-ion batteries (LIBs) play an important role in our daily life with a variety of applicants. To this day, significant resources have been dedicated to the development of high-performance LIBs, particularly the research necessary to identify the optimum electrolyte materials to solve the safety issue. Up to this point polymer electrolytes are widely investigated for their potential to improve batteries’ safety. Given the relative high ionic conductivity, λ, around 10-3 S/cm, poly-ethylene oxide (PEO) is frequently utilized as the polymer matrix in this scenario. But compared to the commercial liquid electrolyte, the ionic conductivity of polymer electrolyte needs to be improved for at least ten times. It is widely acknowledged that the transportation of Li+ is directly related to the segmental and backbone motions of the polymer indicating to improve the ionic conductivity by structure optimization of polymer. Instead of using the traditional trial and error method, modern innovative studies intend to develop a microscopic picture of the Li–ion transportation process to instruct the polymer optimization but it is difficult with in-house laboratory methods. This project aims at designing a polymer with high ionic conductivity. To achieve this goal, the microscopic view of Li+ transportation in polymer will be elucidated through molecular dynamics (MD) simulation and the polymer dynamics will be clarified with MD simulation and Quasi-elastic Neutron Scattering (QENS).

Mots clés : mechanism of li ion transportation, ionic conductivity, polymer dynamics, md simulation, neutron scattering, lithium ion battery

Participants :
- Forschungszentrum Jülich (Allemagne) — Coordinator, beneficiary, Recherche, subvention : 189687.36 €