Role of myeloid cells in vascular endothelial growth factor-independent tumor angiogenesis

Area of Science:

• Oncology
• Immunology
• Angiogenesis Research

Background:

• Vascular endothelial growth factor (VEGF) pathway targeting is crucial for cancer and neovascular disorder therapies.
• Resistance to anti-VEGF drugs can lead to cancer recurrence.
• Understanding resistance mechanisms is vital for improving treatment efficacy.

Purpose of the Study:

• To review recent findings on the role of myeloid cells in resistance to anti-VEGF therapies.
• To explore how myeloid cells contribute to refractoriness and acquired resistance.
• To identify potential therapeutic targets within myeloid cell-mediated resistance.

Main Methods:

• Literature review of recent findings on myeloid cells and anti-VEGF resistance.
• Analysis of studies implicating myeloid cell types in tumor angiogenesis.
• Examination of molecular mechanisms, including cytokine signaling and protein factors.

Main Results:

• Tumor-associated macrophages, Tie2-expressing monocytes, and neutrophils are implicated in tumor angiogenesis.
• CD11b+Gr1+ myeloid cells can induce tumor refractoriness to VEGF blockade.
• The protein Bv8, upregulated by granulocyte colony-stimulating factor, mediates this refractory effect.

Conclusions:

• Myeloid cell-dependent proangiogenic mechanisms are key to understanding tumor angiogenesis.
• These findings highlight myeloid cells as significant contributors to anti-VEGF therapy resistance.
• Targeting myeloid cell functions presents promising therapeutic avenues for overcoming resistance.