Our research team investigates how chromatin regulates the response to replication fork (RF) damage and how its disruption contributes to cancer. Many cancers, such as pediatric high-grade gliomas (pHGG), exhibit abnormal DNA repair, resistance to therapies, and mutations in chromatin-related genes, yet the underlying mechanisms remain poorly understood. Building on advanced tools to study RF damage and repair in mammalian cells, we focus on cancer-associated mutations in histone genes and novel chromatin factors involved in this process. Our goal is to uncover how these alterations affect genome integrity and promote tumor cell survival, ultimately advancing our understanding of chromatin’s role in cancer biology.
We aim to address fundamental questions:
Although significant knowledge has been gained over the past decades, we still lack a comprehensive understanding of how chromatin and its related factors trigger proteomic, metabolic, and post-translational modifications (PTMs) at sites of DNA damage detected during DNA synthesis, and how these modifications regulate DNA damage recognition, activation of repair pathways, and faithful duplication of the (epi)genome.
We use CRISPR-Cas9 to modify or knock out specific genes in human cells. It allows us to dissect the roles of individual chromatin-related genes in DNA damage response.
We use microscopy to capture and analyze large numbers of cells rapidly. This method helps visualize and quantify cellular events at the chromatin level.
We employ specialized proteomic techniques to analyze protein composition and modifications from our preferred chromatin-realted proteins.
