Preuss Resident Research Award: bone marrow-derived Flk-1-expressing CD34+ cells contribute to the endothelium of tumor vessels in mouse brain.

Abstract

Angiogenesis is required for sustained neoplastic growth (3). The sprouting of new vessels from the pre-existing vasculature supplies a proliferating mass of hypoxic tumor cells with oxygen and nutrients. Glioblastoma multiforme is one such tumor, characterized by extensive vascular growth and remodeling. A permissive microenvironment coupled with tissue hypoxia, which promotes elaboration of the angiopoietins and vascular endothelial growth factor (VEGF), is implicated in tumor neovascularization. Angiopoietins seem to stimulate recruitment of bone marrow¡Vderived endothelial precursor cells, and VEGF induces myeloproliferation and increases circulating levels of endothelial progenitor cells (2) and also contributes to neo-angiogenesis. The receptor to which VEGF binds, Flk-1 (the mouse variant of the human KDR), is expressed on endothelial cells and helps trigger vascular proliferation when activated.

Cite this paper

@article{Santarelli2005PreussRR, title={Preuss Resident Research Award: bone marrow-derived Flk-1-expressing CD34+ cells contribute to the endothelium of tumor vessels in mouse brain.}, author={Justin G. Santarelli and Vikram M. Udani and Chris Yu Yee Yung and Samuel H. Cheshier and Amy J. Wagers and Rolf A Brekken and Irith Weissman and Victor C K Tse}, journal={Clinical neurosurgery}, year={2005}, volume={52}, pages={384-8} }