Author/Authors :
Phung، نويسنده , , Thuy L. and Ziv، نويسنده , , Keren and Dabydeen، نويسنده , , Donnette and Eyiah-Mensah، نويسنده , , Godfred and Riveros، نويسنده , , Marcela and Perruzzi، نويسنده , , Carole and Sun، نويسنده , , Jingfang and Monahan-Earley، نويسنده , , Rita A. and Shiojima، نويسنده , , Ichiro and Nagy، نويسنده , , Janice A. and Lin، نويسنده , , Michelle I. and Walsh، نويسنده , , Kenneth and Dvorak، نويسنده , , Ann M. and Briscoe، نويسنده , , David M. and Neeman، نويسنده , , Michal and Sessa، نويسنده , , William C. and Dvorak، نويسنده , , Harold F. and Benjamin، نويسنده , , Laura E.، نويسنده ,
Abstract :
Summary
elial cells in growing tumors express activated Akt, which when modeled by transgenic endothelial expression of myrAkt1 was sufficient to recapitulate the abnormal structural and functional features of tumor blood vessels in nontumor tissues. Sustained endothelial Akt activation caused increased blood vessel size and generalized edema from chronic vascular permeability, while acute permeability in response to VEGF-A was unaffected. These changes were reversible, demonstrating an ongoing requirement for Akt signaling for the maintenance of these phenotypes. Furthermore, rapamycin inhibited endothelial Akt signaling, vascular changes from myrAkt1, tumor growth, and tumor vascular permeability. Akt signaling in the tumor vascular stroma was sensitive to rapamycin, suggesting that rapamycin may affect tumor growth in part by acting as a vascular Akt inhibitor.
