Our Research Projects

A central goal in cancer research is to understand how tumor cells acquire and maintain genomic instability, a defining hallmark that drives tumor evolution and therapeutic resistance. By uncovering the molecular mechanisms that safeguard or disrupt genome integrity, such as errors in mitosis, defects in autophagy, and the pathways controlling chromosomal instability, we aim to identify new vulnerabilities that can be leveraged to develop more precise and effective cancer therapies.

How does autophagy–lysosome activity safeguard mitosis and prevent chromosomal instability?

Autophagy and lysosomes are central degradative pathways that maintain cellular homeostasis, yet their functions during mitosis remain largely unexplored. Our laboratory investigates how these pathways support the structural, metabolic, and quality‑control demands of cell division. By defining how autophagy and lysosomal activity protect mitotic progression, we aim to uncover previously overlooked mechanisms that safeguard chromosome segregation and prevent the emergence of chromosomal instability (CIN). This work positions degradative pathways as critical, and understudied, regulators of genome integrity, offering new angles for the development of CIN‑targeted cancer therapies.

Biomarkers of Chromosomal Instability

Our lab investigates how replication stress shapes CIN outcomes and how autophagy modulates this response. Severe replication stress drives senescence in untransformed cells, yet tumor cells often recover and resume proliferation, accumulating additional genomic alterations. We focus on the role of replication‑origin firing during this recovery and its therapeutic potential. In parallel, we explore how autophagy and lysosomes protect mitotic progression, connecting replication stress responses with CIN‑targeted treatment strategies.

How do cancer cells manage replication stress, and how does this process drive chromosomal instability?

We characterize structural nuclear alterations as indicators of genome instability, with a special focus on the toroidal nucleus, a distinctive nuclear phenotype emerging from mitotic defects. We aim to establish this structure as a robust and accessible CIN biomarker for cancer research.

Technological Transfer

Evaluation of the efficiency of natural compounds for skin depigmentation based on their capacity to modulate autophagy

Reference: 311473
Funding: Bella Aurora Labs. S.A
From 15/12/2021 to 15/08/2022
PI: Caroline Mauvezin

Identification of compounds for skin depigmentation based on modulation of autophagy

Reference: 310921
Funding: Bella Aurora Labs. S.A
From 02/10/2020 to 02/02/2021
PI: Albert Tauler and Caroline Mauvezin