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TSU68, an antiangiogenic receptor tyrosine kinase inhibitor, induces tumor vascular normalization in a human cancer xenograft nude mouse model. | LitMetric

AI Article Synopsis

  • The study explores the potential of TSU68, an antiangiogenic agent, to normalize abnormal tumor blood vessels, which could improve the delivery of cancer-fighting drugs.
  • TSU68 was tested on mice with tumors, leading to a significant decrease in interstitial fluid pressure and an increase in pericyte coverage, indicating healthier blood vessels.
  • The findings suggest that TSU68 effectively prunes and reduces the size of tumor vessels, supporting the idea that it can enhance the efficacy of combined cancer therapies.

Article Abstract

Purpose: Combination therapy using antiangiogenic and cytotoxic agents is a useful strategy for advanced cancer, but the mechanism has not yet been elucidated. Moreover, there is a persistent paradox that destroying tumor vasculature with antiangiogenic agents disturbs the delivery of cytotoxic agents. It has been hypothesized that antiangiogenic agents can lead to normalization of tumor vessels that are structurally and functionally abnormal. The normalization means enhancing the deliver of cytotoxic agents. Our purpose was to investigate whether TSU68, a multiple receptor tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2 (VEGFR2), platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR), would induce the normalization of tumor vessels.

Methods: TSU68 was administered for 7 days to mice with xenografted tumors. Tumors of interstitial fluid pressure (IFP) were measured before and after administration of agents. Immunofluorescence double staining for CD31 and alpha-SMA was performed, and a medical video endoscopy system with narrowband illumination (NBI) was used to visualize the vascular pattern.

Results: TSU68 treatment decreased IFP significantly. Immunofluorescence double staining showed a significant increase in the fraction of pericyte coverage in the TSU68-treated group. NBI endoscopy showed that many tumor vessels in TSU68-treated mice were pruned and the diameters of remaining vessels were reduced.

Conclusion: The data supported our hypothesis of tumor vascular normalization by the antiangiogenic agent TSU68.

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Source
http://dx.doi.org/10.1007/s00595-009-4020-yDOI Listing

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