Profile of Diana Passaro, head of “Leukemia & Niche Dynamics” team
Her background
Diana Passaro’s scientific training has been shaped by the study of the mechanisms underlying the initiation and progression of acute leukemias.
During her PhD at the Institut Curie, she investigated the cellular and molecular determinants that confer leukemic cells with self-renewal capacity and resistance to therapy.
Her work demonstrated that these properties are not solely defined by classical phenotypic markers, but rather arise from dynamic cellular states governed by specific signaling pathways.
This conceptual advance reinforced the idea that leukemic “stemness” depends on a network of regulatory processes controlling adhesion, migration, and interactions with the bone marrow niche.
She continued this line of research at the Francis Crick Institute, where she developed intravital imaging approaches and established bone marrow models enabling direct observation of the leukemic niche.
Her postdoctoral work revealed vascular alterations characteristic of acute leukemias and demonstrated their role in tumor progression and poor therapeutic response. This contribution opened important translational perspectives, including the development of imaging tools to quantify bone marrow vascular status as an indicator of prognosis or treatment response.
Overall, her postdoctoral trajectory consolidated expertise at the interface of stem cell biology, advanced imaging, and bioengineering applied to the study of the leukemic microenvironment.
Her research focus areas
Since 2020, Diana Passaro has led the “Leukemia & Niche Dynamics” team at the Institut Cochin, where she investigates how acute leukemias remodel their vascular niche and exploit these changes to sustain disease maintenance.
Her group examines endothelial compartment heterogeneity, leukemia-induced alterations, and the molecular pathways supporting leukemic expansion or resistance to therapy.
By combining multi-omics analyses, murine models, and functional imaging, the team aims to identify microenvironmental determinants that promote disease progression.
From a more translational perspective, her laboratory develops humanized bone marrow organoids and organ-on-chip systems that enable controlled recapitulation of the human vascular niche.
These models provide a powerful framework to study leukemia–endothelium crosstalk and to test strategies targeting microenvironment-specific vulnerabilities.
The team also investigates mechanisms of leukemic dissemination, particularly central nervous system infiltration in T-cell acute lymphoblastic leukemia, to understand how vascular barriers are breached.
Through this integrated approach, her group contributes to redefining the role of the bone marrow niche in leukemia and to identifying novel therapeutic avenues aimed at restoring a microenvironment supportive of normal hematopoiesis.