- Home Page
- Latest Updates
- Tumor Types
- Molecular Causes of Cancer
- Biological Pathways
- Therapeutic Targets
- Pipeline Molecules
- Research Education
- Research ADCs
- Research Apoptosis
- Research B cell
- Research BRAF
- Research HDIs
- Research Hedgehog
- Research HER Pathways
- Research VEGF
- Why is the VEGF ligand essential throughout tumor development?
- What are the strategies for inhibiting the VEGF pathway?
- What are the effects of direct VEGF ligand inhibition?
- Why is continued VEGF inhibition important?
- Why do tumors progress?
- The role of VEGF across tumor types
- Slide decks and videos
- Glossary
- Clinical Trials
- Resources
- Contact Us
Biooncology R-VEGF
Related Resources for this page:
- Clinical Trials
- Future Directions
- Antibody-Drug Conjugates
- HER Signaling
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- VEGF and MVD
- VEGF in bladder cancer
- VEGF in gastric cancer
- VEGF in pancreatic cancer
- VEGF and prognosis
- VEGF and prognosis in multiple myeloma
- VEGF and prognosis in pancreatic cancer
- VEGF and progression
- VEGF and progression in urothelial carcinoma
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF expression and liver metastases
- VEGF expression in gastric cancer
- VEGF expression in multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Glycoengineered Antibodies
- HER Signaling
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- VEGF and MVD
- VEGF in bladder cancer
- VEGF in gastric cancer
- VEGF in pancreatic cancer
- VEGF and prognosis
- VEGF and prognosis in multiple myeloma
- VEGF and prognosis in pancreatic cancer
- VEGF and progression
- VEGF and progression in urothelial carcinoma
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF expression and liver metastases
- VEGF expression in gastric cancer
- VEGF expression in multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Non-Antibody Biologics
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- What are the strategies for inhibiting the VEGF pathway?
- VEGF and MVD
- VEGF in bladder cancer
- VEGF in gastric cancer
- VEGF in pancreatic cancer
- VEGF and prognosis
- VEGF and prognosis in multiple myeloma
- VEGF and prognosis in pancreatic cancer
- VEGF and progression
- VEGF and progression in urothelial carcinoma
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF expression and liver metastases
- VEGF expression in gastric cancer
- VEGF expression in multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Targeted Small Molecules
- Resisting apoptosis
- HER1/EGFR as a therapeutic target
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- Therapeutic potential of HER pathways
- Slide decks and videos
- What are the strategies for inhibiting the VEGF pathway?
- VEGF and MVD
- VEGF in bladder cancer
- VEGF in gastric cancer
- VEGF in pancreatic cancer
- VEGF and prognosis
- VEGF and prognosis in multiple myeloma
- VEGF and prognosis in pancreatic cancer
- VEGF and progression
- VEGF and progression in urothelial carcinoma
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF expression and liver metastases
- VEGF expression in gastric cancer
- VEGF expression in multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Traditional Monoclonal Antibodies
- Anti-EGFL7
- Glossary
- HER Signaling
- HER1/EGFR as a therapeutic target
- HER2:HER3 dimer
- HER2 as a therapeutic target
- HER3 as a therapeutic target
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- Angiogenic Signaling
- Therapeutic potential of HER pathways
- Slide decks and videos
- What are the strategies for inhibiting the VEGF pathway?
- VEGF and MVD
- VEGF in bladder cancer
- VEGF in gastric cancer
- VEGF in pancreatic cancer
- VEGF and prognosis
- VEGF and prognosis in multiple myeloma
- VEGF and prognosis in pancreatic cancer
- VEGF and progression
- VEGF and progression in urothelial carcinoma
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF expression and liver metastases
- VEGF expression in gastric cancer
- VEGF expression in multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Antibody-Drug Conjugates
Video
Full VEGF & angiogenesis
View video now
Slides
The role of VEGF in glioblastoma multiforme (GBM)
View SlidesLinks
VEGF and angiogenesis in glioblastoma
— Oka et al.1
...The VEGF signaling pathway plays an important role in gliomagenesis and activation is closely related with brain tumor development via vascular formation, observations that coincide with our finding that VEGF promoted tumor angiogenesis resulting in rapid growth of [glioblastoma].
Glioblastoma is the most common primary malignant type of brain tumor in adults. Despite aggressive therapy, the average survival time of a patient with glioblastoma is less than 1 year, with a 5-year survival rate of approximately 5%.2 Glioblastoma displays vascular and endothelial cell proliferation, and therefore, blocking angiogenesis (new vessel formation) has been suggested as a potential means to inhibit glioblastoma growth.3,4
Vascular endothelial growth factor (VEGF) has been implicated as a central mediator of angiogenesis in glioblastoma. In vitro and in vivo studies have confirmed a correlation between tumor grade and VEGF expression in gliomas. Additionally, studies in animal models have shown that inhibiting VEGF function inhibits growth of glioma cells in vivo and causes regression of blood vessels.3
In this section, you will find information on the implications of VEGF in glioblastoma, including evidence to support the prevalence of VEGF expression in glioblastoma, as well as the potential role of VEGF as a prognostic factor.
For more information on a specific topic regarding VEGF in glioblastoma, click on the links below.
In This Section
References:
- 1.
- Oka N, Soeda A, Inagaki A, et al. Biochem Biophys Res Commun. 2007;360:553-559.
- 2.
- Steiner H, Karcher S, Mueller M, et al. J NeuroOnc. 2004;66:129-138.
- 3.
- Maity A, Pore N, Lee J, et al. Cancer Res. 2000;60:5879-5886.
- 4.
- Kim KJ, Li B, Winer J, et al. Nature. 1993;362(6423):841-844.