HSC are defined by their quiescent state, their self-renewal and multipotential properties, that are regulated through a combination of intrinsic and extrinsic factors.

Genetic studies have unveiled the implication of transcription factors or of signaling pathways in HSC characteristics but the understanding of the connecting networks between those different pathways in normal hematopoiesis or in leukemic transformation still requires additional work.

Our laboratory is interested to understand the networks that connect these pathways in normal and malignant hematopoiesis

Genotoxic stress, in particular those generated through reactive oxygen species (ROS), induce cellular transformations, in particular in in hematopoietic cells. Hematopoiesis in adults is localized in the BM. HSC and progenitors are in close contact with specialized structures called "niches". These BM niches allow HSC to be maintained in quiescence and their perturbation can induce major deregulations in blood cell production. Intrinsic and extrinsic factors that regulate normal hematopoiesis are, for many of them, implicated into leukemic transformation. Recent publications clearly indicate that the deregulation of pathways, such as NOTCH for instance, in a niche component can induce haematological disorders.

Our laboratory is interested to learn more about the interactions between the medullar niche and leukemic blast cells.