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Biooncology R-VEGF
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- VEGF and progression
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- Summary
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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
- 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
- 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
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- Summary
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- PI3K/Akt/mTOR Signaling
- 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
- Traditional Monoclonal Antibodies
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- Glossary
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- High VEGF expression
- Hypoxic tumor environment promotes angiogenesis
- MVD and progression
- Obinutuzumab (GA101)
- Regulation of VEGF expression
- Serum VEGF as a clinical marker
- Summary
- Summary
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- Angiogenic Signaling
- 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
- Antibody-Drug Conjugates
Video
Full VEGF & angiogenesis
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Slides
The role of VEGF in lung cancer
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Prevalence of VEGF-expressing tumors
Studies assessing vascular endothelial growth factor (VEGF) expression in lung cancer utilize a variety of assay techniques, and therefore prevalence rates may vary widely. In general, however, VEGF has been shown to be expressed in the majority of non-small cell lung cancer (NSCLC) tumors.1-3 One study that examined 88 patients with surgically resected non-small cell lung carcinomas found VEGF high expression in4
- 77% (68/88) of all non-small cell lung carcinomas
- 75% (36/48) of squamous cell carcinomas
- 73% (22/30) of adenocarcinomas
- 100% (10/10) of large-cell carcinomas
Interestingly, some NSCLC tumors appear to have a nonangiogenic phenotype. In one study, Passalidou et al reported that approximately 9% (9 of 113) of tumors showed no evidence of neovascularization. It has been hypothesized that such tumors, which fill up in alveoli, acquire their blood supply from adjacent alveolar septa.5
In general, however, NSCLC tumors express VEGF and are highly vascularized, and the intensity of vascularization has been shown to correlate with the probability of metastasis.6
References:
- 1.
- Yuan A, Yu CJ, Chen WJ, et al. Int J Cancer (Pred Oncol). 2000;89:475-483.
- 2.
- Imoto H, Osaki T, Taga S, et al. J Thorac Cardiovasc Surg. 1998;115:1007-1014.
- 3.
- Koukourakis MI, Giatromanolaki A, Thorpe PE, et al. Cancer Res. 2000;60:3088-3095.
- 4.
- Stefanou D, Batistatou A, Arkoumani E, et al. Histol Histopathol. 2004;19:37-42.
- 5.
- Passalidou E, Trivella M, Singh N, et al. Br J Cancer. 2002;86:244-249.
- 6.
- Macchiarini P, Fontanini G, Hardin MJ, et al. Lancet. 1992;340:145-146.