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Angiogenesis in cancer: molecular mechanisms, clinical impact.
- Source :
- Langenbeck's Archives of Surgery; Jul2007, Vol. 392 Issue 3, p371-379, 9p, 1 Color Photograph, 3 Diagrams
- Publication Year :
- 2007
-
Abstract
- Angiogenesis, the formation of new blood vessels from the endothelium of the existing vasculature, is fundamental in tumor growth, progression, and metastasis. Inhibiting tumor angiogenesis is a promising strategy for treatment of cancer and has been successfully transferred from preclinical to clinical application in recent years. Whereas conventional therapeutic approaches, e.g. chemotherapy and radiation, are focussing on tumor cells, antiangiogenic therapy is directed against the tumor supplying blood vessels. This review will summarize important molecular mechanisms of tumor angiogenesis and advances in the design of antiangiogenic drugs. Furthermore, clinical implications of antiangiogenic therapy in surgical oncology will be discussed. First antiangiogenic drugs have been approved for treatment of advanced solid tumors in several countries. Leading antiangiogenic drugs are designed to inhibit vascular endothelial growth factor-mediated tumor angiogenesis. Combining antiangiogenic agents with conventional chemotherapy or radiation is currently investigated clinically with great emphasis to realize a multimodal tumor therapy, targeting both the tumor cell and tumor vascular compartment. Antiangiogenic tumor therapy represents a promising strategy for treatment of cancer and will most likely exhibit its clinical potential in combination with established standard tumor therapies in the future. [ABSTRACT FROM AUTHOR]
- Subjects :
- NEOVASCULARIZATION
CANCER
ENDOTHELIUM
TUMOR growth
DRUG therapy
RADIATION
Subjects
Details
- Language :
- English
- ISSN :
- 14352443
- Volume :
- 392
- Issue :
- 3
- Database :
- Complementary Index
- Journal :
- Langenbeck's Archives of Surgery
- Publication Type :
- Academic Journal
- Accession number :
- 24939817
- Full Text :
- https://doi.org/10.1007/s00423-007-0150-0