Intracellular signaling in tumor and endothelial cells: The expected and, yet again, the unexpected - PubMed (original) (raw)
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Intracellular signaling in tumor and endothelial cells: The expected and, yet again, the unexpected
Oliver Stoeltzing et al. Cancer Cell. 2006 Aug.
Free article
Abstract
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.
Comment on
- Pathological angiogenesis is induced by sustained Akt signaling and inhibited by rapamycin.
Phung TL, Ziv K, Dabydeen D, Eyiah-Mensah G, Riveros M, Perruzzi C, Sun J, Monahan-Earley RA, Shiojima I, Nagy JA, Lin MI, Walsh K, Dvorak AM, Briscoe DM, Neeman M, Sessa WC, Dvorak HF, Benjamin LE. Phung TL, et al. Cancer Cell. 2006 Aug;10(2):159-70. doi: 10.1016/j.ccr.2006.07.003. Cancer Cell. 2006. PMID: 16904613 Free PMC article.
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