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Updated: Sep 16, 2026
A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
Clinical experience with angiogenesis signaling inhibitors: focus on vascular endothelial growth factor (VEGF)
1UCLA Jonsson Cancer Center, Los Angeles, CA 90095-7059, USA. lsrosen@mednet.ucla.edu2
Abstract:
Angiogenesis is required for tumor growth and metastasis and, therefore, represents an exciting target for cancer treatment. Angiogenesis is a complex process that is tightly regulated by pro- and anti-angiogenic growth factors. Physiologic angiogenesis takes place during tissue growth and repair, during the female reproductive cycle, and during fetal development. Pathologic angiogenesis is characterized by either excessive (eg, cancer) or inadequate (eg, coronary artery disease) neovascularization. Angiogenesis occurs in a series of complex and interrelated steps that involve the release of pro-angiogenic growth factors, such as vascular endothelial growth factor (VEGF). VEGF regulates both vascular proliferation and permeability, and functions as an anti-apoptotic factor for newly formed blood vessels. The biological effects of VEGF are mediated by two receptors, VEGF-1 and VEGF-2, whose expression is largely limited to the vascular endothelium. VEGF is often expressed in tumors at substantially increased levels. It is expressed in response to hypoxia, oncogenes, and other cytokines, and its expression is associated with poor prognosis in several types of cancer. Several different strategies have been used to inhibit VEGF, including anti-VEGF monoclonal antibodies (eg, bevacizumab) and agents that inhibit the VEGF receptor (eg, SU5416). Both types of agents have tolerable side effects and have shown promise when evaluated in a wide range of tumor types. Angiogenesis, the role of VEGF in angiogenesis and malignancy, and strategies for cancer treatment with VEGF inhibitors are discussed.
Insights
Tumor growth and metastasis depend on angiogenesis, the formation of new blood vessels. Inhibiting vascular endothelial growth factor (VEGF) offers a promising strategy for cancer treatment.
Area of Science:
- Oncology
- Vascular Biology
- Molecular Medicine
Background:
- Angiogenesis, the formation of new blood vessels, is crucial for tumor growth and metastasis.
- This process is tightly regulated by pro- and anti-angiogenic factors, with vascular endothelial growth factor (VEGF) playing a key role.
- Pathologic angiogenesis can lead to excessive neovascularization in cancer or inadequate vessel formation in diseases like coronary artery disease.
Purpose of the Study:
- To explore the role of angiogenesis and vascular endothelial growth factor (VEGF) in cancer development and progression.
- To discuss various strategies for inhibiting VEGF as a therapeutic approach for cancer treatment.
- To review the efficacy and safety of VEGF inhibitors in preclinical and clinical settings.
Main Methods:
- Review of scientific literature on angiogenesis, VEGF signaling pathways, and cancer biology.
- Analysis of studies investigating the expression of VEGF in tumors and its correlation with prognosis.
- Examination of data from clinical trials evaluating VEGF inhibitors, such as monoclonal antibodies and receptor inhibitors.
Main Results:
- VEGF is a critical regulator of vascular proliferation, permeability, and survival of new blood vessels, and its overexpression is linked to poor prognosis in various cancers.
- Inhibitors targeting VEGF, including monoclonal antibodies like bevacizumab and receptor inhibitors like SU5416, have demonstrated potential in treating a range of tumor types.
- These anti-VEGF strategies generally exhibit tolerable side effect profiles.
Conclusions:
- Targeting angiogenesis, particularly through VEGF inhibition, represents a significant therapeutic strategy for combating cancer.
- VEGF inhibitors have shown promise in clinical evaluations, offering a new avenue for cancer treatment.
- Further research and development of VEGF-targeted therapies are warranted to improve patient outcomes in oncology.
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