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Targeting inflammatory cells to improve anti-VEGF therapies in oncology

Hans-Peter Gerber1, Ezogelin Olazoglu, Iqbal S Grewal

  • 1Sr Dir Discovery Tumor Prog, Pharma, Research & Development, Pearl River, NY, USA. gerberh@wyeth.com

Recent Results in Cancer Research. Fortschritte Der Krebsforschung. Progres Dans Les Recherches Sur Le Cancer
|December 25, 2009
PubMed

Insights

Tumor resistance to anti-VEGF therapies involves inflammatory cells like myeloid-derived suppressor cells and macrophages. Targeting these cells may improve cancer treatment strategies.

Area of Science:

  • Oncology
  • Immunology
  • Angiogenesis Research

Background:

  • Vascular endothelial growth factor A (VEGF-A) is crucial for angiogenesis, making it a target for cancer therapies.
  • Tumor resistance to anti-VEGF treatments is a significant clinical challenge.
  • Tumor angiogenesis involves inflammatory cells, including myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs).

Purpose of the Study:

  • To review inflammatory components regulating tumor angiogenesis.
  • To examine the role of inflammatory cells in mediating refractoriness to anti-VEGF therapy.
  • To discuss therapeutic strategies targeting inflammatory pathways in tumor angiogenesis.

Main Methods:

  • Literature review of inflammatory cells and angiogenesis.
  • Analysis of mechanisms of anti-VEGF treatment resistance.
  • Discussion of therapeutic interventions targeting inflammatory cells.

Main Results:

  • CD11b+Gr1+ myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) are key inflammatory cells mediating refractoriness to anti-VEGF treatment.
  • These inflammatory cells contribute to tumor angiogenesis and treatment resistance.
  • Understanding these inflammatory components is vital for improving anti-VEGF therapies.

Conclusions:

  • Inflammatory cells significantly impact tumor angiogenesis and resistance to anti-VEGF therapies.
  • Targeting inflammatory pathways offers potential strategies to overcome treatment refractoriness.
  • Further research into these mechanisms can enhance the efficacy of anti-cancer treatments.

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