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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
- 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 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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 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
Summary: VEGF in gastric cancer
VEGF is a potent proangiogenic factor released by many solid tumors, and the large majority of gastric carcinomas have elevated levels of VEGF.1-3 As a clinical marker, sVEGF levels have been found to be significantly higher in gastric cancer patients than in controls (P<0.0001). sVEGF levels are significantly correlated with disease stage, (P=0.01) and with distant metastases (P=0.004).4
High VEGF expression is characteristic of gastric carcinomas,5 where VEGF and other growth factors form an autocrine loop.6 A significant relationship exists between VEGF expression and MVD in gastric cancers (P=0.008), where MVD was found to be elevated by 46% in VEGF-positive tumors.7 High MVD has been associated with an increased risk of metastases. Tumors positive for VEGF are associated with increased risk of hepatic metastases.8,9
Prognostically, VEGF expression is associated with shorter overall survival time, as well as diminished disease-free survival.3 Positive correlations exist between MVD and VEGF expression.3 MVD has been found to be an independent risk factor for survival in gastric carcinoma, where significant differences in overall survival have been found between patients with low and high MVD (P<0.001).7
References:
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- Suzuki S, Dobashi Y, Hatakeyama Y, et al. BMC Cancer. 2010;10:659.
- 2.
- Nagy JA, Feng D, Vasile E, et al. Lab Invest. 2006;86:767-780.
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- Fondevila C, Metges JP, Fuster J, et al. Br J Cancer. 2004;90:206-215.
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- Karayiannakis AJ, Syrigos KN, Polychronidis A, et al. Ann Surg. 2002;236:37-42.
- 5.
- Kösem M, Tuncer I, Kotan Ç, et al. Hepatogastroenterology. 2009;56:1236-1240.
- 6.
- Smith MG, Hold GL, Tahara E, et al. World J Gastroenterol. 2006;12:2979-2990.
- 7.
- Zhao HC, Qin R, Chen XX, et al. World J Gastroenterol. 2006;12:7598-7603.
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- Maeda K, Chung YS, Ogawa Y, et al. Cancer. 1996;77:858-863.
- 9.
- Tanigawa N, Amaya H, Matsumura M, et al. Cancer Res. 1996;56:2671-2676.