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They have also been proposed to facilitate tumor spread through the blood or lymphatic vasculature 3.

Furthermore, blood vessels have angiocrine capacity supporting directly the growth of tumors through the production of cytokines and growth factors 2. It is classically proposed that for tumor progression to occur new blood vessels must form that will allow the provision of oxygen and nutrients, however these vessels also provide beneficial roles by allowing immune cells and drug delivery to inhibit tumor growth 1. Tumor vascularization is one of the hallmarks of cancer. The understanding of endothelial heterogeneity opens new avenues for more effective anti-vascular therapies in cancer. Functionally, EVPs did not rely on VEGF-A signaling whereas endothelial-specific loss of Rbpj depleted the population and strongly inhibited metastasis. Molecular profiling by RNA sequencing of purified endothelial fractions characterized EVPs as quiescent progenitors remodeling the extracellular matrix with significant paracrine activity promoting growth. These cells harbored self-renewal and reactivated the expression of SOX18 transcription factor, initiating a vasculogenic process as single cells, progressing towards a transit amplifying stage and ultimately differentiating into more mature endothelial phenotypes that comprised arterial, venous and lymphatic subtypes within the core of the tumor. Using fate-mapping analysis of endothelial cell populations in melanoma, we report the very early infiltration of endovascular progenitors (EVP) in growing tumors. Current anti-angiogenic therapies have limited success prompting the need to better understand the cellular origin of tumor vessels.

Tumor vascularization is a hallmark of cancer central to disease progression and metastasis.

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