Abstract
The emergence of vascular disrupting agents (VDAs) is a significant advance in the treatment of solid tumors. VDAs induce rapid and selective shutdown of tumor blood flow resulting in massive necrosis. However, a viable marginal tumor rim always remains after VDA treatment and is a major cause of recurrence. In this review, we discuss the mechanisms involved in the resistance of solid tumors to VDAs. Hypoxia, tumor-associated macrophages, and bone marrow-derived circulating endothelial progenitor cells all may contribute to resistance. Resistance can be monitored using magnetic resonance imaging markers. The various solutions proposed to manage tumor resistance to VDAs emphasize combining these agents with other approaches including antiangiogenic agents, chemotherapy, radiotherapy, radioimmunotherapy, and sequential dual-targeting internal radiotherapy.
Highlights
The emergence of small molecule agents that target the tumor vasculature is an advance in the treatment of malignant solid tumors [1,2,3]
We summarize the mechanisms involved in the resistance of solid tumors to vascular disrupting agents (VDAs), the role of imaging markers in visualizing and understanding resistance, and the various solutions proposed to overcome tumor resistance to VDAs
The results demonstrated the high targetability of 131I-hypericin to tumor necrosis by in vivo single-photon emission computed tomography
Summary
The emergence of small molecule agents that target the tumor vasculature is an advance in the treatment of malignant solid tumors [1,2,3]. In a rat liver xenograft tumor model treated with ZD6126, Chen et al [12] found that VDA treatment did not induce a significant increase in CEPs or www.impactjournals.com/oncotarget plasma SDF-1α 4 hours or 2 days following therapy.
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