Angiogenesis: a curse or cure?
- 1Division of Hematology, Oncology and Transplantation, University of Minnesota Medical School, Minneapolis, USA
- 2Department of Surgery, Shanghai Cancer Hospital, Fudan University, Shanghai, China and Fred Hutchinson Cancer Research Center, Public Health Science, Seattle, Washington, USA
- Correspondence to: Dr K Gupta Division of Hematology, Oncology and Transplantation, University of Minnesota Medical School, Mayo Mail Code 480, 420 Delaware Street SE, Minneapolis, Minnesota 55455, USA; gupta014umn.edu
- Received 21 April 2004
- Accepted 25 August 2004
Abstract
Angiogenesis, the growth of new blood vessels is essential during fetal development, female reproductive cycle, and tissue repair. In contrast, uncontrolled angiogenesis promotes the neoplastic disease and retinopathies, while inadequate angiogenesis can lead to coronary artery disease. A balance between pro-angiogenic and antiangiogenic growth factors and cytokines tightly controls angiogenesis. Considerable progress has been made in identifying these molecular components to develop angiogenesis based treatments. One of the most specific and critical regulators of angiogenesis is vascular endothelial growth factor (VEGF), which regulates endothelial proliferation, permeability, and survival. Several VEGF based treatments including anti-VEGF and anti-VEGF receptor antibodies/agents are in clinical trials along with several other antiangiogenic treatments. While bevacizumab (anti-VEGF antibody) has been approved for clinical use in colorectal cancer, the side effects of antiangiogenic treatment still remain a challenge. The pros and cons of angiogenesis based treatment are discussed.
- EC, endothelial cell
- ECM, extracellular matrix
- VEGF, vascular endothelial growth factor
- VPF, vascular permeability factor
- FGF, fibroblast growth factor
- PLGF, placenta derived growth factor
- TSP, thrombospondin
- PEDF, pigment epithelium derived growth factor
- MMP, matrix metalloproteinases
- COX-2, cycloxygenase-2
- AMD, age related macular degeneration
- PTK, protein tyrosine kinase
- HIF, hypoxia inducible transcription factor
Footnotes
-
Funding: this work was supported by a National Institutes of Health grant (HL68802-01) and a Susan G Komen Breast Cancer Foundation grant to KG.
-
Conflicts of interest: none declared.







