Cytotoxicity of VEGF121/rGel on vascular endothelial cells resulting in inhibition of angiogenesis is mediated via VEGFR-2
2011

VEGF121/rGel: A Targeted Therapy for Tumor Blood Vessels

publication 10 minutes Evidence: high

Author Information

Author(s): Mohamedali Khalid A, Ran Sophia, Gomez-Manzano Candelaria, Ramdas Latha, Xu Jing, Kim Sehoon, Cheung Lawrence H, Hittelman Walter N, Zhang Wei, Waltenberger Johannes, Thorpe Philip E, Rosenblum Michael G

Primary Institution: The University of Texas M. D. Anderson Cancer Center

Hypothesis

The fusion protein VEGF121/rGel targets and destroys tumor neovasculature by specifically affecting endothelial cells that overexpress VEGFR-2.

Conclusion

VEGF121/rGel selectively targets and kills endothelial cells overexpressing VEGFR-2, inhibiting angiogenesis without affecting normal blood vessels.

Supporting Evidence

  • VEGF121/rGel was found to bind specifically to VEGFR-2 but not to VEGFR-1.
  • VEGF121/rGel demonstrated a 100-fold difference in cytotoxicity between cells expressing VEGFR-2 and those expressing VEGFR-1.
  • Treatment with VEGF121/rGel completely inhibited bFGF-stimulated neovascular growth in chicken chorioallantoic membranes.

Takeaway

This study shows that a special protein can kill cancer blood vessel cells without hurting normal cells, which could help treat tumors better.

Methodology

The study involved in vitro and in vivo experiments assessing the binding, cytotoxicity, and internalization of VEGF121/rGel in endothelial cells expressing different VEGF receptors.

Potential Biases

Potential bias in the interpretation of results due to the use of specific cell lines and experimental conditions.

Limitations

The study primarily focused on specific cell lines and may not fully represent the complexity of tumor environments in vivo.

Statistical Information

P-Value

p<0.001

Statistical Significance

p<0.001

Digital Object Identifier (DOI)

10.1186/1471-2407-11-358

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