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Presentation

 

To understand epigenetic aberrations in tumor progression, there are few cellular or animal models compared to genetic alterations. This discrepancy is large due to the plasticity of epigenetic modifications. Inducing a desired epigenetic modification at  a given location in the genome remains a challenge. In the team, we seek to understand the dynamics of acquisition of epigenetic alterations during tumorigenesis, to evaluate their stability over time and to characterize their link with the tumor phenotype. These questions are prerequisites for using these alterations as therapeutic targets.

To understand epigenetic aberrations in tumor progression, there are few cellular or animal models compared to genetic alterations. This discrepancy is largely due to the plasticity of epigenetic modifications. Inducing a desired epigenetic modification at a given location in the genome remains a challenge. In the team, we seek to understand the dynamics of acquisition of epigenetic alterations during tumorigenesis, to evaluate their stability over time and to characterize their link with the tumor phenotype. These questions are prerequisites for using these alterations as therapeutic targets.

The lab studies focus on non-genetic mechanisms of breast tumor evolution during the early phases of tumor initiation and in response and resistance to cancer treatment. We are developing experimental and computational approaches to map epigenomic marks at single-cell resolution, allowing the study of chromatin mark dynamics in tumor samples (Grosselin et al. Nat Genet 2019; Prompsy et al. Nat Comm 2020). On our latest results, we combined single-cell epigenomic and transcriptomic approaches to lineage tracing strategies and reveal initial epigenomic events driving chemotherapy tolerance in triple-negative breast cancer (Marsolier & Prompsy et al ., Nat Genet 2022), demonstrating that the repressive histone mark H3K27me3 is a lock to the activation of a drug-persistent expression program in breast cancers, paving the way for a therapeutic rationale for combining chemotherapy with histone demethylase inhibitors.

One of the strengths of our team is the in-depth expertise in both data mining and molecular biology.

We develop bioinformatics and statistical analyzes to characterize and model the epi-transcriptomic states encountered. Our laboratory has expertise in cancer epigenetics and single-cell epigenomic technology. We are recognized worldwide for our ability to profile histone modifications in human tumors with single-cell resolution, using its high-throughput single-cell ChIP-seq technique.
Team Vallot was created at the Institut Curie in 2017 and brings together both wet lab specialists in epigenetics and computational scientists to constitute a multidisciplinary team of 12 people.

The team is SiRIC (Integrated Cancer Research Site) certified and supported by the ATIP – Avenir program, an ERC Starting Grant and recipient of 9 national awards for research innovation, and we regularly participate in international scientific events (e.g. Gordon Conferences, EMBO, ESMO).

France Culture: program “la Méthode Scientifique” 2021
Céline Vallot – Epimédicaments

CNRS: Movie about the lab for the CNRS Bronze Medal 2018
Céline Vallot – Bronze Medal CNRS 2018

France Culture: program “la Méthode Scientifique” 2017
Céline Vallot- Epigénétique reportage

 

 

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