- 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
- A brief history of ADCs
- Current research in ADCs
- Cytotoxic agent
- 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
- 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 in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- What are ADCs?
- Antibody-Drug conjugates
- Glycoengineered Antibodies
- 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 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 in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Targeted Small Molecules
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Multiple Myeloma
- PI3K Inhibitor (GDC-0941)
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
- Summary
- Summary
- PI3K/Akt/mTOR Signaling
- 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 in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Vismodegib (GDC-0449) Smoothened Inhibitor
- Traditional Monoclonal Antibodies
- Glossary
- 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
- 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 in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Antibody-Drug Conjugates
VEGF expression in multiple myeloma
VEGF plays a significant role in the pathogenesis of multiple myeloma, affecting various biological processes.1
Studies have revealed that VEGF is secreted directly by myeloma cells and that VEGF secretion was markedly upregulated when myeloma cells bind to bone marrow stromal cells. It has also been found that VEGF stimulates proliferation in both endothelial and stromal cells (via VEGFR-2 and VEGFR-1 signaling, respectively) and is correlated with increased angiogenesis in bone marrow.1-3
In a study that compared the VEGF levels between solitary plasmacytoma, a localized bone disease that can be a precursor of multiple myeloma, and multiple myeloma, Swelam and Tamimi analyzed 10 histopathologically representative cases from each disease category (chosen from the 50 initial samples collected in each group) and found that VEGF expression was significantly higher (P<0.01) in multiple myeloma tissues compared with tissues of solitary plasmacytoma.4,5
VEGF expression in multiple myeloma vs solitary plasmacytoma4
The same study also showed that VEGF activity is not restricted to endothelial cells, but is also found in tumor cells.4
Adapted from Swelam WM, Tamimi DM. Pathol Res Pract. 2010;206:753-759. Diagram 1.
Immunohistochemistry showing VEGF in multiple myeloma (A) and solitary plasmacytoma (B)4
Reprinted with permission from Swelam WM, Tamimi DM. Pathol Res Pract. 2010;206:753-759. Figure 2.
References:
- 1.
- Le Gouill S, Podar K, Amiot M, et al. Blood. 2004;104:2886-2892.
- 2.
- Gupta D, Treon SP, Shima Y, et al. Leukemia. 2001;15:1950-1961.
- 3.
- Vacca A, Ria R, Ribatti D, et al. Haematologica. 2003;88:176-185.
- 4.
- Swelam WM, Tamimi DM. Pathol Res Pract. 2010;206:753-759.
- 5.
- Canger EM, Celenk P, Alkan A, Günhan O. Med Oral Patol Oral Cir Bucal. 2007;12:E7-E9.