TY - JOUR
T1 - Intracellular signaling in tumor and endothelial cells
T2 - The expected and, yet again, the unexpected
AU - Stoeltzing, Oliver
AU - Meric-Bernstam, Funda
AU - Ellis, Lee M.
N1 - Funding Information:
Supported by the German Cancer Society (Deutsche Krebshilfe, Max Eder Program, Bonn, Germany) (O.S.), NIH grant R01 CA112199 (F.M.-B.), and NIH R01 CA112390 (L.M.E.). The authors apologize to those whose important contributions to the field could not be cited due to the restriction on the number of references.
PY - 2006/8
Y1 - 2006/8
N2 - In this issue of Cancer Cell, Phung and coworkers demonstrate that sustained endothelial activation of Akt by expression of constitutively activated Akt1 (myrAkt1) leads to blood vessels that essentially recapitulate the complex structural and functional abnormalities of tumor vessels. The authors provide evidence that rapamycin inhibition of PI3K/Akt/mTOR signaling in endothelial cells (ECs), by either reducing Akt activity or blocking mTOR, reverses the pathologic effects associated with excess VEGF signaling in the tumor vasculature. However, unexpected findings following mTOR inhibition in vivo highlight the seemingly paradoxical and complex effects of rapamycin on various cell types within the tumor microenvironment.
AB - In this issue of Cancer Cell, Phung and coworkers demonstrate that sustained endothelial activation of Akt by expression of constitutively activated Akt1 (myrAkt1) leads to blood vessels that essentially recapitulate the complex structural and functional abnormalities of tumor vessels. The authors provide evidence that rapamycin inhibition of PI3K/Akt/mTOR signaling in endothelial cells (ECs), by either reducing Akt activity or blocking mTOR, reverses the pathologic effects associated with excess VEGF signaling in the tumor vasculature. However, unexpected findings following mTOR inhibition in vivo highlight the seemingly paradoxical and complex effects of rapamycin on various cell types within the tumor microenvironment.
UR - http://www.scopus.com/inward/record.url?scp=33746818291&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33746818291&partnerID=8YFLogxK
U2 - 10.1016/j.ccr.2006.07.013
DO - 10.1016/j.ccr.2006.07.013
M3 - Short survey
C2 - 16904605
AN - SCOPUS:33746818291
SN - 1535-6108
VL - 10
SP - 89
EP - 91
JO - Cancer cell
JF - Cancer cell
IS - 2
ER -