- 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 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
- 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 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
- 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 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
- 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 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
- 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 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
VEGF and angiogenesis in gastric cancer
— Kösem M, Tuncer I, Kotan Ç, et al. Hepato-Gastroenterology. 20091
...VEGF and the angiogenesis promoted by VEGF play important roles in cancer growth, infiltration and metastasis in gastric carcinoma.
Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic factors discovered to date. It is a signaling molecule secreted by many solid tumors.2,3 High VEGF expression is seen in many human cancer cells, and is also expressed in stromal cells, particularly at sites of relative hypoxia.3-5 VEGF promotes endothelial cell proliferation and migration, and induces angiogenesis.6,7 As its other name—vascular permeability factor (an earlier term for the protein)—suggests, VEGF increases vascular permeability to plasma and its proteins, a characteristic of tumor microvasculature.3
Gastric cancers are overwhelmingly sporadic malignancies, developing in people without a high-risk germ-line mutation.8,9 Adenocarcinomas predominate in the stomach in more than 95% of malignancies. The majority of these express VEGF as an angiogenic factor that results in neovascularization within carcinomas. According to the Lauren classification, these neoplasms are described as intestinal or diffuse types. Intestinal tumors are glandular in nature, while the less common diffuse tumors lack cohesion and functionality.9
Gastric cancer was ranked as the fourth most common global malignancy in 2008, with an estimated 989,600 new cases. About 738,000 people worldwide died from gastric cancer in 2008.10 Gastric carcinoma grows aggressively and, following total gastrectomy, the cancer recurs in nearly 30% of patients.11 Among patients with advanced gastric carcinoma, only 30% are expected to survive 5 or more years after curative resection.12
This section highlights VEGF expression in gastric cancer, as well as the role of VEGF in gastric tumor progression, increased microvessel density (MVD), and malignant metastases.
For more information on a specific topic regarding VEGF and angiogenesis in gastric cancer, click on the links below.
References:
- 1.
- Kösem M, Tuncer I, Kotan Ç, et al. Hepatogastroenterology. 2009;56:1236-1240.
- 2.
- Suzuki S, Dobashi Y, Hatakeyama Y, et al. BMC Cancer. 2010;10:659.
- 3.
- Nagy JA, Feng D, Vasile E, et al. Lab Invest. 2006;86:767-780.
- 4.
- Murat A, Migliavacca E, Hussain SF, et al. PLoS One. 2009;4:e5947.
- 5.
- Pinto MP, Badtke MM, Dudevoir ML, et al. Cancer Res. 2010;70:2655-2664.
- 6.
- Zhao HC, Qin R, Chen XX, et al. World J Gastroenterol. 2006;12:7598-7603.
- 7.
- Wang S, Li X, Parra M, et al. Proc Natl Acad Sci U S A. 2008;105:7738-7743.
- 8.
- National Cancer Institute dictionary of genetics terms: http://www.cancer.gov/cancertopics/genetics/genetics-terms-alphalist/all.
Accessed May 16, 2011. - 9.
- Smith MG, Hold GL, Tahara E, et al. World J Gastroenterol. 2006;12:2979-2990.
- 10.
- American Cancer Society. Global cancer facts & figures, 2nd edition, 2011. http://www.cancer.org/acs/groups/content/@epidemiologysurveilance/
documents/document/acspc-027766.pdf. Accessed July 15, 2011. - 11.
- Maeda K, Chung YS, Ogawa Y, et al. Cancer. 1996;77:858-863.
- 12.
- Tanigawa N, Amaya H, Matsumura M, et al. Cancer Res. 1996;56:2671-2676.