- 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
- 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
- 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 multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- What are ADCs?
- Antibody-Drug conjugates
- 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 multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Non-Antibody Biologics
- Apoptosis
- 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 multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Targeted Small Molecules
- Apoptosis
- Gastric Cancer
- 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 multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Traditional Monoclonal Antibodies
- Glossary
- Gastric Cancer
- 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
- Angiogenic 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 multiple myeloma
- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
- VEGF, MVD, and metastases in gastric carcinoma
- Antibody-Drug Conjugates
Share
VEGF expression in gastric cancer1
Different levels of VEGF expression in gastric carcinoma (a and b).
Reprinted with permission from Oh SY, Kwon HC, Kim SH, et al. BMC Cancer. 2008;8:123. Figure 1.
As one of the key proangiogenic factors secreted by many solid tumor types,2 elevated levels of VEGF have also been found in the majority of gastric adenocarcinomas.3
Expression of VEGF, serum VEGF, and other proangiogenic factors were studied by Oh et al, who examined 114 specimens of gastric cancer obtained from curative gastrectomies. By immunohistochemical analyses, high VEGF expression was seen in 57.9% of specimens, significantly more frequently in specimens from patients ≥60 years of age (P=0.013) and in intestinal type tumors (P=0.014).1
References:
- 1.
- Oh SY, Kwon HC, Kim SH, et al. BMC Cancer. 2008;8:123.
- 2.
- Suzuki S, Dobashi Y, Hatakeyama Y, et al. BMC Cancer. 2010;10:659.
- 3.
- Fondevila C, Metges JP, Fuster J, et al. Br J Cancer. 2004;90:206-215.