Vascular function is tightly regulated by structural and architectural cues. Several functional abnormalities in the bone marrow (BM) vasculature have been reported. Particularly, vascular wall barriers responsible of oxygen, nutrients and drug delivery are severely damaged, with increased permeability, altered perfusion and release of healthy stem cells (HSCs) to periphery. High throughput RNA-sequencing analysis of BM-derived endothelial cells (ECs) have shown multiple molecular alterations (Passaro et al., Cancer Cell 2017).

Of particular interest, in the presence of AML engraftment a dramatic change in the expression of several adhesion molecules involved in cell migration, interaction with extra cellular matrix (ECM) and survival of newly forming vessels takes place. We and others have reported that leukemic stem cell function responsible of disease initiation and drug resistance is dependent on interaction with the microenvironment (Passaro et al., Cancer Cell 2015). Thus, we are interested in understanding how the pathologic remodeling of adhesion molecules in the endothelium mediated the leukemia interaction with the vascular niche to support leukemia growth.