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VEGF in tumor progression and targeted therapy

Vladimir P Chekhonin1, Sergey A Shein, Anna A Korchagina

  • 1Department of Medicinal Nanobiotechnologies, N.I. Pirogov Russian National Research Medical University, Russia, Moscow.

Current Cancer Drug Targets
|November 22, 2012
PubMed

Insights

Vascular endothelial growth factor A (VEGF-A) blockade inhibits tumor growth but is controversial for high-grade gliomas. Multi-target strategies are needed to overcome resistance and enhance anti-VEGF therapy efficacy.

Area of Science:

  • Oncology
  • Cancer Biology
  • Translational Medicine

Background:

  • Tumor progression relies on vascularization and angiogenesis, with vascular endothelial growth factor A (VEGF-A) being a key proangiogenic factor.
  • VEGF-A blockade, exemplified by bevacizumab, is used in treating various cancers, including breast and colorectal cancers, and recurrent high-grade gliomas (HGGs).
  • While bevacizumab can improve progression-free survival and quality of life, its efficacy in brain tumors like HGGs is debated due to limited recovery and potential for enhanced invasion.

Purpose of the Study:

  • To evaluate the role of anti-VEGF therapy in solid tumor progression, particularly in high-grade gliomas (HGGs).
  • To explore the challenges and resistance mechanisms associated with anti-VEGF therapy in HGGs.
  • To propose multi-target strategies for enhancing antitumor treatment efficacy beyond VEGF-A inhibition.

Main Methods:

  • Review of existing clinical practices and research on anti-VEGF therapies, including bevacizumab.
  • Analysis of mechanisms of resistance to anti-VEGF therapy in HGGs.
  • Discussion of alternative and complementary therapeutic strategies.

Main Results:

  • Anti-VEGF therapy can inhibit tumor vascularization and growth but shows controversial efficacy in HGGs, offering only modest delay and not complete recovery.
  • Resistance mechanisms include alternative proangiogenic pathways, invasive tumor cell populations, metabolic shifts to glycolysis, and recruitment of myeloid cells.
  • Anti-VEGF antibodies show potential as drug delivery vectors for brain tumors.

Conclusions:

  • Anti-VEGF therapy as monotherapy is insufficient for HGGs.
  • A multi-target strategy is essential to inhibit angiogenesis, invasion, autophagy, metastasis, and the recruitment of specific cell types.
  • Anti-VEGF antibodies may serve as valuable vectors for targeted drug and diagnostic delivery in brain tumors.

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