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Biooncology R-VEGF
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- 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
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
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- 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
- Resisting apoptosis
- HER1/EGFR as a therapeutic target
- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
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- Summary
- Therapeutic potential of HER pathways
- 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
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- High VEGF expression
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- 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
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Full VEGF & angiogenesis
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The role of VEGF in glioblastoma multiforme (GBM)
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VEGF and tumorigenesis
Oka et al evaluated in vitro and in vivo effects of VEGF on the properties of cancer stem cells (CSCs) derived from human glioblastomas. Evidence from previous studies had suggested that CSCs are found in malignant tumor cells and play a pivotal role in tumor initiation, growth, and recurrence. Oka at el demonstrated that VEGF did not affect the property of CSCs in vitro. However, the injection of mouse brains with VEGF-expressing CSCs led to massive expansion of vascular-rich glioblastoma and was associated with high morbidity. Based on these results, the authors suggested that VEGF promotes tumorigenesis via angiogenesis and that VEGF induces the proliferation of vascular endothelial cells in the vascular-rich tumor environment of glioblastoma.1,2
Kaplan–Meier survival curve showing the rapid onset of high tumor-induced morbidity. All mice injected with EGFP-VEGF-X01GB cells showed signs of tumor-induced morbidity within 64 days post-injection; mice injected with EGFP-X01GB (without VEGF) did not. The mean survival after EGFP-VEGF-X01GB injection was 57 days; mice injected with EGFP-X01GB survived for a mean of 81 days (P=0.0005; hazard ratio (HR)=4.470 (95% CI, 3.505–84.81).1
Adapted from Biochemical and Biophysical Research Communications, Vol 360, Oka N. et al, VEGF Promotes Tumorigenesis and Angiogenesis of Human Glioblastoma Stem Cells, Page 553-559, Copyright 2007, with permission from Elsevier.
References:
- 1.
- Oka N, Soeda A, Inagaki A, et al. Biochem Biophys Res Commun. 2007;360:553-559.
- 2.
- Calabrese C, Poppleton H, Kocak M, et al. Cancer Cell. 2007;11(1):69-82.