Dr Ficara conducted graduate studies in hematopoietic stem cell (HSC) biology and gene therapy at the OSR-TIGET, Milan, Italy. After obtaining a PhD in Immunology, she moved to Stanford University, US. As a postdoc, Dr Ficara discovered that in healthy HSCs the PBX1 oncoprotein maintains quiescence and restrains myeloid maturation while preserving lymphoid and erhythroid potential.

She later joined Humanitas Research Hospital to generate hematopoietic progenitors from iPSCs for regenerative medicine purposes. Dr Ficara now holds a permanent position with the National Research Council (CNR) and leads a research group in Humanitas. Her efforts focus on how the self-renewal/differentiation balance is maintained in HSCs, since alterations of this equilibrium leads to hematological disorders, through the study of transcription factors, micro-RNAs and interaction with the bone marrow niche. Her lab discovered that miR-127 acts as a brake for myeloid differentiation, contributing to preserve HSC long-term self-renewal.

More recently, Dr Ficara studied HSCs in the context of myeloproliferative neoplasm (MPN), as a paradigm of diseases initiated by mutated stem cells, to explore novel therapeutic options. Her lab generated a mouse model in which the JAK2-V617F MPN-driver mutation is induced without PBX1. This tool allowed to show that PBX1 is a key player in establishing and maintaining MPN, and to identify other potential MPN contributors, which are currently under investigation.