Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo
Abstract
The development of new blood vessels (angiogenesis) is required for many physiological processes including embryogenesis, wound healing and corpus luteum formation. Blood vessel neoformation is also important in the pathogenesis of many disorders, particularly rapid growth and metastasis of solid tumours. There are several potential mediators of tumour angiogenesis, including basic and acidic fibroblast growth factors, tumour necrosis factor-alpha and transforming factors-alpha and -beta. But it is unclear whether any of these agents actually mediates angiogenesis and tumour growth in vivo. Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen and an angiogenesis inducer released by a variety of tumour cells and expressed in human tumours in situ. To test whether VEGF may be a tumour angiogenesis factor in vivo, we injected human rhabdomyosarcoma, glioblastoma multiforme or leiomyosarcoma cell lines into nude mice. We report here that treatment with a monoclonal antibody specific for VEGF inhibited the growth of the tumours, but had no effect on the growth rate of the tumour cells in vitro. The density of vessels was decreased in the antibody-treated tumours. These findings demonstrate that inhibition of the action of an angiogenic factor spontaneously produced by tumour cells may suppress tumour growth in vivo.
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In 1993, anti-VEGF monoclonal antibodies significantly reduced vessel density and delayed tumor growth in nude mice carrying rhabdomyosarcoma, glioblastoma multiforme, and leiomyosarcoma xenografts.
“In 1993, it was reported that treatment with anti‐VEGF monoclonal antibodies resulted in a significant reduction in vessel density and a significant delay in tumor growth in nude mice carrying rhabdomyosarcoma, glioblastoma multiforme (GBM), and leiomyosarcoma xenografts.”
From Hypoxia signaling in cancer: Implications for therapeutic interventions (2023) · cites this paper as [266]
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- Authors
- Kim, K. J., Li, B., Winer, J., Armanini, M., Gillett, N., Phillips, H. S., & Ferrara, N.
- Affiliations
- Genentech (US)
- Venue
- Nature
- Published
- 1993-04
- Volume
- 362
- Issue
- 6423
- Pages
- 841-844
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1969328947
- Cited by
- 3,605
- References
- 32
- Citations by year
- 2026: 22 · 2025: 25 · 2024: 43 · 2023: 47 · 2022: 53 · 2021: 55 · 2020: 55 · 2019: 54 · 2018: 89 · 2017: 101 · 2016: 81 · 2015: 78 · 2014: 98 · 2013: 110 · 2012: 137
- FWCI
- 32.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- vascular endothelial growth factor, angiogenesis, tumor angiogenesis, tumor growth inhibition, monoclonal antibodies, rhabdomyosarcoma, glioblastoma, leiomyosarcoma, tumor vasculature, nude mice, tumour metastasis
- MeSH terms
- Animals, Antibodies, Monoclonal, Cell Division, Female, Glioblastoma, Humans, Leiomyosarcoma, Lymphokines, Mice, Nude, Neoplasm Transplantation, Neoplasms, Experimental, Neovascularization, Pathologic, Rhabdomyosarcoma, Tumor Cells, Cultured, Endothelial Growth Factors, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Mice
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