Normalizing tumor vasculature with anti-angiogenic therapy: A new paradigm for combination therapy
By Rakesh K. Jain. Nature Medicine, 2001
2,258 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/662ede05471c630328a9990a6b30076a23352f06
How researchers see this paper
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In Cancer Research
- Rakesh K. Jain
- N. Ferrara
- J. Joyce
- D. Hanahan
- Triantafyllos Stylianopoulos
- Peter Carmeliet
- Dai Fukumura
- John D. Martin
In Molecular Biology
- Rakesh K. Jain
- J. Joyce
- N. Ferrara
- Dai Fukumura
- Peter Carmeliet
- D. Hanahan
- Triantafyllos Stylianopoulos
- D. McDonald
In Oncology
- Rakesh K. Jain
- J. Joyce
- N. Ferrara
- Triantafyllos Stylianopoulos
- Dai Fukumura
- D. Hanahan
- John D. Martin
- Peter Carmeliet
Citations in the corpus
- Inhibition of vascular endothelial growth factor (VEGF) signaling in cancer causes loss of endothelial fenestrations, regression of tumor vessels, and appearance of basement membrane ghosts. (2004, background): “VEGF/VEGFR inhibition can decrease the diameter, tortuosity, and permeability of tumor vessels(28) and even transform surviving tumor vessels into a more normal phenotype.(32,33) Considering the important role of VEGF and its receptors in regulating vascular function, we sought to characterize the c”
- Delivering nanomedicine to solid tumors (2010, background): “Therefore, judicious application of antiangiogenic agents can restore the balance and revert the vasculature to a more 'normal' phenotype”
- Lessons from phase III clinical trials on anti-VEGF therapy for cancer (2006, background): “To resolve this paradox, in 2001 we proposed that anti-VEGF therapy can 'normalize' tumor vasculature”
- Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer (2004, background): “The carboxyl-terminal domain (111-165) of vascular endothelial growth factor is critical for its mitogenic potency.”
- Kinetics of vascular normalization by VEGFR2 blockade governs brain tumor response to radiation: role of oxygenation, angiopoietin-1, and matrix metalloproteinases. (2004, background): “In theory, reducing or abolishing vascular studies have demonstrated an additive tumor growth delay, abnormalities by anti-VEGF therapy should “normalize” the tuothers have shown a stronger, synergistic effect (Teicher et al., mor vasculature and alleviate hypoxia (Jain, 2001).”