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Biooncology R-VEGF
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- VEGF and MVD
- VEGF in bladder cancer
- VEGF in gastric cancer
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- 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
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
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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
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- VEGF in multiple myeloma
- VEGF pathways in multiple myeloma
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- What are the strategies for inhibiting the VEGF pathway?
- VEGF and MVD
- VEGF in bladder cancer
- VEGF in gastric cancer
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- 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
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- What are the strategies for inhibiting the VEGF pathway?
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- 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
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Full VEGF & angiogenesis
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The role of VEGF in ovarian cancer
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VEGF-mediated angiogenesis in the functional reproductive cycle
Recurrent VEGF-mediated angiogenesis followed by vascular regression is unique to the ovulatory cycle and highly regulated.1
New vessel generation is essential for the whole reproductive cycle, and the role of vascular growth factors involved in regulating this process, particularly VEGF, is demonstrated by highly regulated changes in expression throughout an ovulatory cycle.1,2
Hormonal profiles and angiogenic responses during a human ovulatory cycle1
Adapted from Ramakrishnan S, Subramanian IV, Yokyama Y, et al. Angiogenesis. 2005;8:169-182. Figure 2 with permission from Springer Science and Business Media.
Intrafollicular levels of VEGF, in particular VEGF-A, increase during the initial part of the ovulatory cycle, peaking just before the start of the luteal phase.2 Subsequent vascular regression during follicular atresia is promoted by elevated levels of angiogenic inhibitors and reduced VEGF levels toward the end of the luteal phase and the ovulation cycle. LH=luteinizing hormone; FSH=follicle-stimulating hormone; EG-VEGF=endocrine–gland derived-vascular endothelial growth factor.1,2
References:
- 1.
- Ramakrishnan S, Subramanian IV, Yokoyama Y, Geller M. Angiogenesis. 2005;8:169-182.
- 2.
- Kumaran GC, Jayson GC, Clamp AR. Br J Cancer. 2009;100:1-7.