Rapamycin inhibits primary and metastatic tumor growth by antiangiogenesis: involvement of vascular endothelial growth factor

By M. Guba, P. Breitenbuch, M. Steinbauer, G. Koehl, Stefanie Flegel, M. Hornung, C. Bruns, C. Zuelke, S. Farkas, M. Anthuber and 2 more. Nature Medicine, 2002

1,758 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/335f7e06c573eb7de12cc8cbc6170695eb14d3a1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Citations in the corpus

The tor pathway: a target for cancer therapy (2004, background): “Similarly, rapamycin decreased production of Vegf, markedly inhibited the response of vascular endothelial cells to stimulation by Vegf and inhibited metastatic tumour growth in mouse solid-tumour model”
Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer (2009, background): “Rapamycin was found to have anti-angiogenic activities associated with markedly reduced production of VEGF, and it completely abrogated the response of vascular endothelial cells to stimulation by VEG”
Malignancy after Transplantation (2005, background): “CsA-induced production of cytokines such as transforming growth factor (TGF)-beta and/or vascular endothelial growth factor (VEGF) may promote carcinogenesis (40, 41), which may also play a role in promoting tumor development.”
Defining the role of mTOR in cancer. (2007, background): “Angiogenesis A particularly interesting property of rapamycin is its ability to suppress angiogenesis (Guba et al., 2002).”
Natural products for cancer chemotherapy (2011, background): “, 2003) by interfering with angiogenesis (Guba et al., 2002; Pray, 2002) and inducing apoptosis.”
TOR signalling in bugs, brain and brawn (2003, background): “In addition to blocking the growth of tumour cells directly, it also has an indirect effect by preventing the growth of new blood vessels (angiogenesis) that supply oxygen and nutrients to the tumour cell”
Current development of mTOR inhibitors as anticancer agents (2006, background): “Interestingly, all the above factors can activate the PI3K/AKT/mTOR pathway in cancer cells, endothelial cells or pericyte”
Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB. (2006, background): “Rapamycin is known to have antiangiogenic effects (Guba et al., 2002), and we find that the drug strongly inhibits Akt/PKB in endothelial cells (Figure 2D).”
Maintenance Immunosuppression with Target-of-Rapamycin Inhibitors is Associated with a Reduced Incidence of De Novo Malignancies (2005, background): “Another independent study showed that rapamycin reduced VEGF production and decreased the size of hepatic metastases in mice undergoing adenocarcinoma cell injections into the portal vein (11).”
Hypoxia-inducible factor determines sensitivity to inhibitors of mTOR in kidney cancer (2006, background): “In addition to cell-autonomous effects, inhibitors of mTOR have antiangiogenic activity, as growth of endothelial cells is dependent on mTOR in certain setting”
Target of Rapamycin (TOR) in Nutrient Signaling and Growth Control (2011, background): “Rapamycin is effective against tumors because it blocks the growth of tumor cells directly and because of the indirect effect of preventing the growth of new blood vessels (angiogenesis) that supply oxygen and nutrients to the tumor cells (Guba et al. 2002).”