- 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:
- Future Directions
- Antibody-Drug Conjugates
- A brief history of ADCs
- Current research in ADCs
- Cytotoxic agent
- Emerging therapeutic options
- Emerging therapeutic options
- HER Signaling
- High VEGF expression
- How are ADCs designed to work?
- Hypoxic tumor environment promotes angiogenesis
- Glossary
- MVD and progression
- Monoclonal antibody
- Regulation of VEGF expression
- Research ADCs
- Serum VEGF as a clinical marker
- Slide decks and videos
- Stable linker
- Summary
- Summary
- Summary
- Summary
- Targeting cancers with ADCs
- Trastuzumab Emtansine (T-DM1)
- 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
- What are ADCs?
- Antibody-Drug conjugates
- Bispecific Monoclonal Antibodies
- Glycoengineered Antibodies
- Emerging therapeutic options
- Emerging therapeutic options
- 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
- Emerging therapeutic options
- Emerging therapeutic options
- Resisting apoptosis
- HER1/EGFR as a therapeutic target
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MAPK Signaling
- MEK Inhibitor (GDC-0973)
- MVD and progression
- Melanoma
- PI3K Inhibitor (GDC-0941)
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- PI3K/Akt/mTOR 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
- Traditional Monoclonal Antibodies
- Anti-EGFL7
- Glossary
- Emerging therapeutic options
- Emerging therapeutic options
- 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
- Melanoma
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- Angiogenic Signaling
- Inhibition of HER2 dimerization
- 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
Science of VEGF and angiogenesis
View SlidesLinks
Angiogenesis is essential to tumor development
A hallmark of cancer throughout tumor development
While there are more than 100 distinct types of cancer (and considerable heterogeneity within each tumor type), there exists a remarkable similarity in the pathologic traits that collectively drive tumor growth. Across most—if not all—malignancies, sustained angiogenesis is considered to be one of these central hallmarks of cancer.1
Acquired capabilities of cancer2

Reprinted from Hanahan D, Weinberg RA, "The Hallmarks of Cancer: The Next Generation" in Cell, 2011;144:646-674, with permission from Elsevier.
In their seminal review paper, "The Hallmarks of Cancer," and a recent update paper, Hanahan and Weinberg proposed 6 acquired capabilities of cancer cells and gave examples of possible enabling mechanisms.1,2
Angiogenesis is 1 of the 6 cellular transformations that lead to malignant growth
| Acquired Capability | Possible Cancer-enabling Mechanism |
|---|---|
| 1. Sustaining proliferative signaling | Oncogene activation (Activated H-Ras) |
| 2. Resisting cell death | Production of survival growth factors, such as IGF |
| 3. Evading growth suppressors | Disruption of retinoblastoma protein (pRb) pathway |
| 4. Enabling replicative immortality | Gain of telomerase function |
| 5. Inducing angiogenesis | Induction of VEGF production |
| 6. Activating invasion and metastases | Inactivation of E-cadherin |
The establishment of "inducing angiogenesis" as one of the fundamental "hallmarks of cancer" is based on more than a century of research. To learn more about these research milestones, view the History of VEGF research section.
References:
- 1.
- Hanahan D, Weinberg RA. Cell. 2000;100:57-70.
- 2.
- Hanahan D, Weinberg RA. Cell. 2011;144:646-674.