Journal
CANCER CELL
Volume 10, Issue 2, Pages 159-170Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2006.07.003
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Funding
- NCI NIH HHS [P01 CA092644, R01 CA106263, P01 CA09264401, R01 CA109086, R01 CA106263-04, R01 CA109086-04, P01 CA092644-04, CA106263, R01 CA109086-03] Funding Source: Medline
- NHLBI NIH HHS [R01 HL71049-01, T32 HL007893, R01 HL071049, T32 HL07893] Funding Source: Medline
- NIAID NIH HHS [P01 AI50157, R01 AI046756, P01 AI050157] Funding Source: Medline
- NIDDK NIH HHS [T32 DK007726] Funding Source: Medline
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Endothelial 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.
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