Author/Authors :
Calabrese، نويسنده , , Christopher and Poppleton، نويسنده , , Helen and Kocak، نويسنده , , Mehmet and Hogg، نويسنده , , Twala L. and Fuller، نويسنده , , Christine and Hamner، نويسنده , , Blair and Oh، نويسنده , , Eun Young and Gaber، نويسنده , , M. Waleed and Finklestein، نويسنده , , David and Allen، نويسنده , , Meredith and Frank، نويسنده , , Adrian and Bayazitov، نويسنده , , Ildar T. and Zakharenko، نويسنده , , Stanislav S. and Gajjar، نويسنده , , Amar and Davidoff، نويسنده , , Andrew and Gilbertson، نويسنده , , Richard J.، نويسنده ,
Abstract :
Summary
s are believed to arise from cancer stem cells (CSCs), but it is not known if these cells remain dependent upon the niche microenvironments that regulate normal stem cells. We show that endothelial cells interact closely with self-renewing brain tumor cells and secrete factors that maintain these cells in a stem cell-like state. Increasing the number of endothelial cells or blood vessels in orthotopic brain tumor xenografts expanded the fraction of self-renewing cells and accelerated the initiation and growth of tumors. Conversely, depletion of blood vessels from xenografts ablated self-renewing cells from tumors and arrested tumor growth. We propose that brain CSCs are maintained within vascular niches that are important targets for therapeutic approaches.
