5 Critical questions in the science of VEGF and angiogenesis

  1. Question 1 preview icon - “Why is the VEGF ligand essential throughout tumor development?” Why is the VEGF ligand essential throughout tumor development? arrow
  2. Question 2 preview icon - “What are the strategies for inhibiting the VEGF pathway?” What are the strategies for inhibiting the VEGF pathway? arrow
  3. Question 3 preview icon - “What are the effects of direct VEGF ligand inhibition?” What are the effects of direct VEGF ligand inhibition? arrow
  4. Question 4 preview icon - “Why is continued VEGF inhibition important?” Why is continued VEGF inhibition important? arrow
  5. Question 5 preview icon - “Why do tumors progress?” Why do tumors progress? arrow
Why is the VEGF ligand essential throughout tumor development?
The VEGF ligand may play an essential role throughout tumor development by helping tumor vessels establish, grow, and survive1
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What are the strategies for inhibiting the VEGF pathway?
The 2 primary strategies for VEGF pathway inhibition include targeting either the VEGF ligand or the VEGF receptor2
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What are the effects of direct VEGF ligand inhibition?
Direct VEGF ligand inhibition may result in regression of existing tumor vasculature and inhibition of new and recurrent tumor vessel growth3-7
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Why is continued VEGF inhibition important?
Regrowth of tumor vasculature—at a rate consistent with normal tumor development—may occur when VEGF inhibition is stopped8,9
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Why do tumors progress?
Tumor progression may occur through acquired resistance (with agents that target the tumor directly) or through the activation of secondary pathways (with agents that target VEGF directly)10-12
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  1. Why is the VEGF ligand essential throughout tumor development?

  2. What are the strategies for inhibiting the VEGF pathway?

  3. What are the effects of direct VEGF ligand inhibition?

  4. Why is continued VEGF inhibition important?

  5. Why do tumors progress?

References:
1.
Ellis LM, Hicklin DJ. Nat Rev Cancer. 2008;8:579-591. PMID: 18596824
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Hicklin DJ, Ellis LM. J Clin Oncol. 2005;23:1011-1027. PMID: 15585754
3.
Baka S, Clamp AR, Jayson GC. Expert Opin Ther Targets. 2006;10:867-876. PMID: 17105373
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Presta LG, Chen H, O'Connor SJ, et al. Cancer Res. 1997;57:4593-4599. PMID: 9377574
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Jain RK, Duda DG, Clark JW, Loeffler JS. Nat Clin Pract Oncol. 2006;3:24-40. PMID: 16407877
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Borgström P, Hillan KJ, Sriramarao P, Ferrara N. Cancer Res. 1996;56:4032-4039. PMID: 8752175
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Borgström P, Bourdon MA, Hillan KJ, et al. Prostate. 1998;35:1-10. PMID: 9537593
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Lee CG, Heijn M, di Tomaso E, et al. Cancer Res. 2000;60:5565-5570. PMID: 11034104
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Willett CG, Boucher Y, di Tomaso E, et al. Nat Med. 2004;10:145-147. PMID: 14745444
10.
Yuan F, Chen Y, Dellian M, et al. Proc Natl Acad Sci U S A. 1996;93:14765-14770. PMID: 8962129
11.
Mancuso MR, Davis R, Norberg SM, et al. J Clin Invest. 2006;116:2610-2621. PMID: 17016557
12.
Aita M, Fasola G, Defferrari C, et al. Crit Rev Oncol Hematol. 2008;68:183-196. PMID: 18606548
13.
Sweeney CJ, Miller KD, Sledge GW. Trends Mol Med. 2003;9:24-29. PMID: 12524207
14.
Ton NC, Jayson GC. Curr Pharm Des. 2004;10:51-64. PMID: 14754405
15.
Bergers G, Hanahan D. Nat Rev Cancer. 2008;8:592-603. PMID: 18650835

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