What we do
In many adult epithelia multiple cell types are renewed throughout the life by specific pools of stem cells. While maintaining their lineage identity, stem cells and their differentiated progeny tightly crosstalk to assure the right
tissue homeostasis. The skin is a physical, chemical and immunological barrier from the outside environment. When injured, such as during wound healing, different cell lineages at different differentiation state, participate to restore
the integrity of the skin through the acquisition of an unexpected plasticity. The concept that inflammatory events occurring during skin regeneration, such as the immune cell infiltration, can contribute to trigger skin cancer onset,
is well established. However, recent studies suggest the existence of common, but yet unknown, transcriptional and chromatin key factors of cell plasticity that control and regulate wound healing and skin cancer onset.
In our lab, we integrate state-of-the-art molecular and cellular biology techniques. In particular we employ in vitro genetic screenings, in vivo bulk and single cell omics analyses and computational methods to identify these key regulatory networks.