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- What are ADCs?
- Glycoengineered Antibodies
- VEGF expression in gastric cancer
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- High VEGF expression
- VEGF and prognosis in multiple myeloma
- MVD and progression
- Hypoxic tumor environment promotes angiogenesis
- Serum VEGF as a clinical marker
- Regulation of VEGF expression
- VEGF expression in multiple myeloma
- VEGF pathways in multiple myeloma
- Summary
- VEGF and progression
- VEGF in bladder cancer
- VEGF in pancreatic cancer
- Summary
- Summary
- VEGF and MVD
- Summary
- VEGF and prognosis
- VEGF and prognosis in pancreatic cancer
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF and progression in urothelial carcinoma
- VEGF in gastric cancer
- VEGF in multiple myeloma
- Non-Antibody Biologics
- Apoptosis
- VEGF expression in gastric cancer
- High VEGF expression
- VEGF and prognosis in multiple myeloma
- MVD and progression
- Hypoxic tumor environment promotes angiogenesis
- Serum VEGF as a clinical marker
- Regulation of VEGF expression
- VEGF expression in multiple myeloma
- What are the strategies for inhibiting the VEGF pathway?
- VEGF pathways in multiple myeloma
- Summary
- VEGF and progression
- VEGF in bladder cancer
- VEGF in pancreatic cancer
- Summary
- Summary
- VEGF and MVD
- Summary
- VEGF and prognosis
- VEGF and prognosis in pancreatic cancer
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF and progression in urothelial carcinoma
- VEGF in gastric cancer
- VEGF in multiple myeloma
- Targeted Small Molecules
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- VEGF expression in gastric cancer
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- Regulation of VEGF expression
- VEGF expression in multiple myeloma
- What are the strategies for inhibiting the VEGF pathway?
- VEGF pathways in multiple myeloma
- Summary
- VEGF and progression
- VEGF in bladder cancer
- VEGF in pancreatic cancer
- Summary
- Summary
- VEGF and MVD
- Summary
- VEGF and prognosis
- VEGF and prognosis in pancreatic cancer
- VEGF and tumor progression in gastric cancer
- VEGF and tumor progression in pancreatic cancer
- VEGF and progression in urothelial carcinoma
- VEGF in gastric cancer
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- Traditional Monoclonal Antibodies
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- Regulation of VEGF expression
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- What are the strategies for inhibiting the VEGF pathway?
- VEGF pathways in multiple myeloma
- Summary
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- Summary
- Summary
- VEGF and MVD
- Summary
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- VEGF and prognosis in pancreatic cancer
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Liver Metastases & VEGF Expression1
VEGF levels in liver metastases1
A comparison of VEGF levels in nontumorous liver tissue and liver metastases showing 36.6 ± 10.0 pg/mg protein and 376.8 ± 106.1 pg/mg protein, respectively (Wilcoxon’s signed-rank test: P=0.0016). Twenty-three consecutive patients with metastatic pancreatic adenocarcinoma who received systemic chemotherapy were included in the study. The average age of the study population (14 men and 9 women) was 60 years.1
Reprinted with permission from Tawada K, Ishihara T, Kobayashi A, et al. Clin Cancer Res. 2008;14:7438-7443. Figure 1.
The liver is the most common site for metastases of pancreatic adenocarcinoma. A study by Tawada et al examined VEGF expression in liver metastases and its correlation with VEGF expression in the primary tumor in 23 patients with pancreatic adenocarcinoma and liver metastases. Diagnoses were done using percutaneous needle biopsy of the liver and by endoscopic ultrasonographic fine-needle aspiration of the pancreatic tumor. The VEGF level in liver metastases was significantly greater than in nontumorous liver tissue (P=0.0016). The level in nontumorous tissue was 36.6 ± 10.0 pg/mg (4.2-239.8 pg/mg) protein vs 376.8 ± 106.1 pg/mg (8.7-1,834.9 pg/mg) protein in liver metastases.1
A retrospective study by Seo et al examined tissue samples from 142 patients with ductal pancreatic adenocarcinoma who underwent resection between 1976 and 1997. VEGF expression was found in tumor cells as well as vascular endothelial cells. The incidence of liver metastasis was significantly higher in the group with moderate or strong VEGF expression (P=0.014).2
References:
- 1.
- Tawada K, Ishihara T, Kobayashi A, et al. Clin Cancer Res. 2008;14:7438-7443. PMID: 18974391
- 2.
- Seo Y, Baba H, Fukuda T, et al. Cancer. 2000;88:2239-2245. PMID: 10820344